scholarly journals Monitoring of blood volume during haemodialysis treatment of acute renal and multiple organ failures

1996 ◽  
Vol 11 (supp8) ◽  
pp. 20-23 ◽  
Author(s):  
K. S. Katzarski
2021 ◽  
Vol 16 ◽  
Author(s):  
Ali Fathijouzdani ◽  
Rezvan Heidarimoghadam ◽  
Maryam Hazhirkamal ◽  
Akram Ranjbar

: The COVID-19 pandemic has caused serious concerns for people around the world. The COVID-19 is associated with respiratory failure, generation of reactive oxygen species (ROS), and the lack of antioxidants among patients. Specified ROS levels have an essential role as an adjuster of immunological responses and virus cleaners. Still, excessive ROS will oxidize membrane lipids and cellular proteins and quickly destroy virus-infected cells. It can also adversely damage normal cells in the lungs and even the heart, resulting in multiple organ failures. Given the above, a highly potent antioxidant therapy can be offered to reduce cardiac loss due to COVID-19. In modern medicine, nanoparticles containing antioxidants can be used as a high-performance therapy in reducing oxidative stress in the prevention and treatment of infectious diseases. It can provide a free and interactive tool to determine whether antioxidants & nanoantioxidants can be administered for COVID-19. More research and studies are needed to investigate and make definitive opinions about their medicinal uses.


2019 ◽  
Vol 12 (6) ◽  
pp. e229610
Author(s):  
Hideharu Hagiya ◽  
Futoshi Nakagami ◽  
Yuki Minami ◽  
Hiroaki Terada

We herein describe an irregular case of toxic-shock syndrome (TSS). A previously healthy 28-year-old Japanese man developed a sudden-onset high fever. The patient was suffering from conjunctival hyperaemia, gastrointestinal symptoms such as vomiting and diarrhoea, and systemically diffused macular erythroderma. Further physical examination detected pustules on his back, which self-destructed over time. Laboratory revealed multiple organ failures. Subsequently, scalded skin on the face and desquamation in the limb extremities emerged by day 10, leading to the diagnosis of TSS, despite his stable circulatory dynamics through the course. Learning points for clinicians include that they should recall TSS as a possible disease concurrently causing high fever, systemic rash and multiple organ dysfunctions, even without being in a state of shock. The characteristic desquamations emerged in the limb extremities after hospitalisation were of help in diagnosing TSS.


Author(s):  
John M. Litell ◽  
Nathan I. Shapiro

The pathophysiology of sepsis is the result of a dysregulated host response to infection. Interactions between conserved pathogenic signals and host recognition systems initiate a systemic reaction to local infection. Pro- and anti-inflammatory intermediates and associated coagulatory abnormalities lead to altered macrovascular, microvascular, and mitochondrial function. Uncorrected, these processes yield similar patterns of failure in multiple organ systems. Mortality increases with successive organ failures. Although commonly thought to be a manifestation of impaired renal circulation, septic acute kidney injury may be due primarily to non-haemodynamic factors. Pulmonary parenchymal dysfunction in sepsis also contributes to failures in other organ systems. Sepsis involves complex alterations in myocardial function, vascular tone, and capillary integrity, which are mediated by elevated concentrations of inflammatory cytokines, inducible nitric oxide, and reactive oxygen species, among others. Gut hypomotility and translocation of enteric flora likely contribute to a persistent inflammatory response. This perpetuates the pathophysiological pattern of sepsis, and can lead to the delayed onset of these features in patients with other types of critical illness. The neurological manifestations of sepsis include acquired delirium, which is also probably due to circulatory and inflammatory abnormalities, as well as alterations in cerebral amino acid metabolism. Critical illness-related corticosteroid insufficiency and derangements in glucose metabolism are among the endocrine abnormalities commonly seen in septic patients. Restoration of homeostasis requires early haemodynamic resuscitation and aggressive infectious source control.


2020 ◽  
Vol 7 ◽  
Author(s):  
Francesca Salamanna ◽  
Melania Maglio ◽  
Maria Paola Landini ◽  
Milena Fini

The explosion of the new coronavirus (SARS-CoV-2) pandemic has brought the role of the angiotensin converting enzyme 2 (ACE2) back into the scientific limelight. Since SARS-CoV-2 must bind the ACE2 for entering the host cells in humans, its expression and body localization are critical to track the potential target organ of this infection and to outline disease progression and clinical outcomes. Here, we mapped the physiological body distribution, expression, and activities of ACE2 and discussed its potential correlations and mutal interactions with the disparate symptoms present in SARS-CoV-2 patients at the level of different organs. We highlighted that despite during SARS-CoV-2 infection ACE2-expressing organs may become direct targets, leading to severe pathological manifestations, and subsequent multiple organ failures, the exact mechanism and the potential interactions through which ACE2 acts in these organs is still heavily debated. Further scientific efforts, also considering a personalized approach aimed to consider specific patient differences in the mutual interactions ACE2-SARS-CoV-2 and the long-term health effects associated with COVID-19 are currently mandatory.


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3021-3021
Author(s):  
James N. Frame ◽  
Elaine A. Davis ◽  
Ying Wang ◽  
Mary S. Emmett ◽  
Ashna R. Malapur

Abstract Background: To date, multiple organ failure complicating HIT has been reviewed in a limited patient (pt.) numbers in the medical literature. Objectives: (1) To describe the clinical features of pts. with HIT who developed the failure of ≥ 2 organs termed multiple organ failure syndrome (MOFS); (2) to determine the prevalence/incidence of MOFS HIT in a cohort of CAMC HIT Registry/open heart surgery (OHS) pts. Design: Retrospective case series identified from an IRB-approved HIT Registry. Setting: Tertiary-care medical center. Patients: 19 patients ≥ 18 yrs who presented from 1.1.00 to 12.31.04 with HIT ± thrombo-embolic complications (TEC) confirmed by serological (HPF4 ELISA, GTI) or functional (HIPA) HIT assays during (n=18) or after (n=1) a recent hospitalization with UFH exposure. Mean age: 71 yrs. (range, 49–84); women: 47%. UFH exposure settings (n): CABG alone (6) or with valve replacement (4), valve replacement alone or RV repair (1 each), aortic dissection repair (1), embolectomy or SBO (2 each), Whipple procedure (1; non-CA), atrial fibrillation (1). Measurements: Classification of MOFS: failure of ≥ 2 organs [e.g., brain, GI tract, liver, kidney, heart, lung (due to PE)] as modifications of the methods of Lefering R. et al (2002) and the Society of Thoracic Surgeons National Adult Cardiac Surgery Database, Version 2.52.1; platelet counts, clinical outcomes. Results: The prevalence of MOFS in HIT Registry pts. was 4.7% (19/404). During this time, the incidence of MOFS complicating OHS HIT pts. in the total OHS pts. was 0.12% (13/11,018). HIT was first suspected a mean of 10d (range, 1–38) from initial UFH exposure and a mean of 4.7d (range, <1d-25) after UFH was D/C’d where overall platelet counts [mean, 74x109/L, (range, 22- to 125-)] showed a 66% decrease from baseline [mean, 218 x 109/L, range (95- to 498-)]. At this time, 12 (63%) pts. had thrombocytopenia alone, 7 (37%) pts. had both thrombocytopenia and TEC, and 13 (68%) pts. had a total 19 organ failures (OF).: 1 OF: 8 pts.; 2 OF’s: 4 pts.; and 3 OF’s: 1 pt. At the time HIT was first suspected, the kidney (47%) and brain (32%) were the most frequent sites of organ failure. After the time HIT was first suspected and diagnosed, 17 (89%) pts. had developed ≥ 1 additional new OF: 1 OF: 7 pts.; 2 OF’s: 5 pts.; 3 OF’s: 5 pts. The liver (39%), kidney (23%) and GI tract (19%) were the most frequent sites of new OF’s. The mean/median overall number of organ failures/pt. were 2.6/2.0 (range, 2 to 4). Direct thrombin inhibitor (DTI) therapy was initiated in 17 (90%) at a mean of 2.5d (SD: 4.0) (range, 0–13) from the date HIT was first suspected: lepirudin (9) or Argatroban (8); (2 were not treated due to family wishes or late recognition). Lepirudin was switched to Argatroban in 2 pts. due to worsening renal failure and Argatroban was switched to lepirudin in 2 pts. due to worsening liver failure. The mean length of DTI therapy was 8.8 d (range, 1–20). Compared with non-MOFS HIT Registry pts. (n=395), MOFS HIT pts. had more fatal outcomes [95% (18/19) vs. 11% (45/395); p = 3.2x 10−15], major bleeding events [26% (5/19) vs. 6.3% (25/395); p = 0.008], and amputations [11% (2/19) vs. 1.5% (6/395); p = 0.047]. Conclusions: Although uncommon, MOFS may be the initial manifestation of HIT and is associated with catastrophic outcomes. Compared to non-MOFS HIT pts., MOFS HIT pts. had an increased rate of fatal outcomes, major bleeding events, and rates of amputation. In a subset of HIT pts., MOFS hampered the delivery of utilized DTI’s. Our data also suggest the need for earlier HIT recognition and DTI interventions.


2021 ◽  
Vol 17 (5) ◽  
pp. e1009587
Author(s):  
Shijie Xu ◽  
Na Jiang ◽  
Waqas Nawaz ◽  
Bingxin Liu ◽  
Fang Zhang ◽  
...  

Severe fever with thrombocytopenia syndrome virus (SFTSV) is a tick-borne emerging phlebovirus with high mortality rates of 6.0 to 30%. SFTSV infection is characterized by high fever, thrombocytopenia, leukopenia, hemorrhage and multiple organ failures. Currently, specific therapies and vaccines remain elusive. Suitable small animal models are urgently needed to elucidate the pathogenesis and evaluate the potential drug and vaccine for SFTSV infection. Previous models presented only mild or no pathogenesis of SFTS, limiting their applications in SFTSV infection. Therefore, it is an urgent need to develop a small animal model for the investigation of SFTSV pathogenesis and evaluation of therapeutics. In the current report, we developed a SFTSV infection model based on the HuPBL-NCG mice that recapitulates many pathological characteristics of SFTSV infection in humans. Virus-induced histopathological changes were identified in spleen, lung, kidney, and liver. SFTSV was colocalized with macrophages in the spleen and liver, suggesting that the macrophages in the spleen and liver could be the principle target cells of SFTSV. In addition, histological analysis showed that the vascular endothelium integrity was severely disrupted upon viral infection along with depletion of platelets. In vitro cellular assays further revealed that SFTSV infection increased the vascular permeability of endothelial cells by promoting tyrosine phosphorylation and internalization of the adhesion molecule vascular endothelial (VE)–cadherin, a critical component of endothelial integrity. In addition, we found that both virus infection and pathogen-induced exuberant cytokine release dramatically contributed to the vascular endothelial injury. We elucidated the pathogenic mechanisms of hemorrhage syndrome and developed a humanized mouse model for SFTSV infection, which should be helpful for anti-SFTSV therapy and pathogenesis study.


Author(s):  
Chiara Musiu ◽  
Simone Caligola ◽  
Alessandra Fiore ◽  
Alessia Lamolinara ◽  
Cristina Frusteri ◽  
...  

AbstractInflammatory responses rapidly detect pathogen invasion and mount a regulated reaction. However, dysregulated anti-pathogen immune responses can provoke life-threatening inflammatory pathologies collectively known as cytokine release syndrome (CRS), exemplified by key clinical phenotypes unearthed during the SARS-CoV-2 pandemic. The underlying pathophysiology of CRS remains elusive. We found that FLIP, a protein that controls caspase-8 death pathways, was highly expressed in myeloid cells of COVID-19 lungs. FLIP controlled CRS by fueling a STAT3-dependent inflammatory program. Indeed, constitutive expression of a viral FLIP homolog in myeloid cells triggered a STAT3-linked, progressive, and fatal inflammatory syndrome in mice, characterized by elevated cytokine output, lymphopenia, lung injury, and multiple organ dysfunctions that mimicked human CRS. As STAT3-targeting approaches relieved inflammation, immune disorders, and organ failures in these mice, targeted intervention towards this pathway could suppress the lethal CRS inflammatory state.


2020 ◽  
Vol 14 (10) ◽  
pp. 1138-1145
Author(s):  
Jianxin Tao ◽  
Yunjuan Nie ◽  
Hui Wu ◽  
Liang Cheng ◽  
Yuanwang Qiu ◽  
...  

Introduction: The coronavirus disease 2019 (COVID-19) pandemic is spreading rapidly. Critically ill cases of COVID-19 can rapidly progress to acute respiratory distress syndrome and multiple organ failures. However, no effective drugs have been available till now, leading to more than 300,000 deaths up to 29 April 2020. Here, we present a critically ill case utilizing umbilical cord blood-derived mesenchymal stem cells (UCB-MSCs). Case presentation: A 72-year-old man was admitted, with the diagnosis of COVID-19, ARDS, type-2 diabetes, diabetic nephropathy, renal insufficiency, and hypertension. His clinical condition continually developed to be life-threatening even receiving various treatment options including antiviral therapy and extracorporeal membrane oxygenation. Between 28 February and 8 March 2020, the patient was given 5-time intravenous infusions of UCB-MSCs. His hematological and biochemical indexes, including lymphocytes and renal function improved. Pulmonary static compliance increased significantly and PaO2/FiO2 ratio maintained stable. On March 10, he received lung transplantation. Conclusions: Our current findings suggested that UCB-MSCs therapy may show some positive effect in treating critical COVID-19 to some extent, for its delaying deterioration of the disease and efficacy in respiratory and renal function, though limited.


2021 ◽  
Vol 20 (4) ◽  
pp. 55-63
Author(s):  
Yu.V. Korotchaeva ◽  
◽  
N.L. Kozlovskaya ◽  
E.M. Shifman ◽  
V.M. Guryeva ◽  
...  

Objective. To study the risk factors for transformation of pre-eclampsia (PE) into atypical hemolytic uremic syndrome (aHUS). Patients and methods. The study included 102 patients with PE, who were divided into two groups. The main group consisted of 59 women with PE and aHUS in the early postpartum period. In the comparison group, there were 43 patients who previously had severe PE, which was not complicated by the development of aHUS. Results. The complications associated with severe PE such as hemorrhage (76.3% vs 48.8%, p = 0.004), placental abruption (33.9% vs 6.9%, p = 0.001), and intrauterine fetal demise (32.2% vs 6.9%, p = 0.002) were significantly more frequent in patients with aHUS compared with the control group. Most of these complications occurred in patients in whom PE lasted more than one week. Also, patients with aHUS had significantly more severe microangiopathic hemolytic anemia (hemoglobin 61.0 [52.5; 73.5] g/L vs 88.0 [73.0; 104.0] g/L, p < 0.001, lactate dehydrogenase 2846.0 [1340.5; 5037.5] IU/L vs 801.0 [497.0; 1269.0] IU/L, p < 0.001), thrombocytopenia (49.5 [31.0; 71.5] K/μL vs 67.0 [43.0; 108.0] K/μL, p = 0.002), hypercreatininemia (424.5 [281.0; 605.0] μmol/L vs 99.0 [86.0; 134.0] μmol/L, p < 0.001) and more severe multiple organ dysfunction syndrome (average number of organ failures – 3.58 vs 1.88, p < 0.001). Among patients with aHUS, complete recovery of renal function was achieved in 42 (71.2%) of 59 women, 9 (15.2%) of 59 women remained on hemodialysis, 8 (13.6%) of 59 women died. In the comparison group, all women showed positive dynamics within 72 hours after childbirth with normalization of all clinical and laboratory parameters. Conclusion. PE itself is a risk factor for the development of aHUS, and patients with severe PE should be considered at high risk for thrombotic microangiopathy. Prolongation of pregnancy in patients with PE increases the risk of developing aHUS by 5 times. Key words: pre-eclampsia, pregnancy-associated atypical hemolytic uremic syndrome, pregnancy, thrombotic microangiopathy, eculizumab


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