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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemodialysis (HD) of infants with end-stage renal disease (ESRD) is technically difficult and labor intensive, although there are few data in the literature to document the outcomes of this treatment. We retrospectively reviewed all patients with ESRD who received HD between 1983 and 1997 who weighed <10 kg at the beginning of HD. A total of ten patients aged 2-27 months, weighing 3.5-9.5 kg, were identified. All patients were dialyzed through a central venous line; three had a failed sapheno-femoral loop and one a failed brachial shunt. Line clot was observed in nine and line sepsis in six patients. Subclavian vein stenosis was documented in one patient following removal of a clotted subclavian line. The mean urea reduction ratios calculated during the 1st and 3rd month of HD were only 54% and 49%, respectively. Anemia was a frequent problem, despite the use of erythropoietin in seven of the infants. Outcomes included: successful renal transplant in four, switch back to peritoneal dialysis in two, improved renal function and dialysis discontinuation in one, and death after withdrawal of treatment in three patients. All three patients who died were <5 months of age, weighed <5 kg, and were anuric; two of the three had congenital nephrotic syndrome. In conclusion, successful HD is possible in small children with ESRD, but morbidity is substantial and mortality is high.
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PMID:Hemodialysis for end-stage renal disease in children weighing less than 10 kg. 1041 60

Involvement of neutrophils in the control of blood parasites in malaria has been reported. Both, mononuclear phagocytes and neutrophils are known to be stimulated by cytokines such as TNF-alpha in order to augment the defence potency against the parasites. Previously, it has been shown that serum-G-CSF concentrations are increased in patients with bacterial sepsis. In vitro studies have shown that P. falciparum - infected erythrocytes induce the release of G-CSF by several cells such as endothelial cells and monocytes, however, nothing is known about G-CSF serum concentrations during the clinical course of severe P. falciparum malaria. Thus, it was the aim of the present study to investigate the time course for G-CSF serum concentrations in patients with complicated P. falciparum malaria, and to correlate these values with other mediators of inflammation and hematopoesis. Twenty-six patients suffering from complicated P. falciparum malaria were included in the study, and 20, age and sex matched, healthy volunteers were used as the negative control group. Serum samples for determination of G-CSF were taken on day 0, 7 and 14, and measured by ELISA. We found significantly increased serum concentrations of G-CSF in patients with complicated P. falciparum malaria on day 0, values decreasing to within the normal range by day 7. A significant correlation was found between G-CSF (d0) and procalcitonin, the parasite count, erythropoietin and macrophage inflammatory protein, however no correlation could be shown for the neutrophil count. In conclusion, on the day of hospital admission, elevated serum concentrations of G-CSF were detected in patients with complicated P. falciparum malaria, which might indicate a role of G-CSF in the acute defence mechanism against the parasites.
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PMID:Serum concentrations of granulocyte-colony stimulating factor in complicated Plasmodium falciparum malaria. 1070 2

Eosinophilia is common in the neonatal period. However, its causes, pathomechanism and clinical significance are still unknown. Previous reports have described that eosinophilia may be associated with numerous conditions (establishment of an anabolic state, drug reactions, response to foreign antigens, chronic lung disease, erythropoietin treatment and infections). The aim of this study was to evaluate the possible association of various conditions, especially infection, with eosinophilia and to clarify whether recognition of increase in eosinophil count is of any clinical significance in the management of a sick neonate. Fifty-six neonates with eosinophilia (absolute eosinophil count > 700/mm3) and 55 control neonates matched for gestational age, birth weight and hospitalization days were included in the study. A significant difference between the two groups was found only in blood transfusions, immuno-globulin treatment, specific antibiotic treatment and infectious disease. However, neonates who develop sepsis and are treated with antibiotics and immuno-globulin are more often transfused. It can thus be concluded that the main relationship observed is between eosinophilia and infection whereas the other associations are secondary. The relative risk factor for infection when the absolute eosinophil count is > 700/mm3, is 1.58, with a confidence interval 1.30-1.91. Eosinophilia seems to be a reliable indicator of sepsis while normal absolute eosinophil count does not exclude infection. Infection should be strongly considered in the evaluation of a sick neonate with eosinophilia.
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PMID:Eosinophilia in sick neonates. 1224 53

Sepsis with acute organ dysfunction (severe sepsis) results from a systemic proinflammatory and procoagulant response to infection. Organ dysfunction in the patient with sepsis is associated with increased mortality. Although most organs have discrete anatomical boundaries and carry out unified functions, the hematologic system is poorly circumscribed and serves several unrelated functions. This review addresses the hematologic changes associated with sepsis and provides a framework for prompt diagnosis and rational drug therapy. Data sources used include published research and review articles in the English language related to hematologic alterations in animal models of sepsis and in critically ill patients. Hematologic changes are present in virtually every patient with severe sepsis. Leukocytosis, anemia, thrombocytopenia, and activation of the coagulation cascade are the most common abnormalities. Despite theoretical advantages of using granulocyte colony-stimulating factor to enhance leukocyte function and/or circulating numbers, large clinical trials with these growth factors are lacking. Recent studies support a reduction in the red blood cell transfusion threshold and the use of erythropoietin treatment to reduce transfusion requirements. Treatment of thrombocytopenia depends on the cause and clinical context but may include platelet transfusions and discontinuation of heparin or other inciting drugs. The use of activated protein C may provide a survival benefit in subsets of patients with severe sepsis. The hematologic system should not be overlooked when assessing a patient with severe sepsis. A thorough clinical evaluation and panel of laboratory tests that relate to this organ system should be as much a part of the work-up as taking the patient's blood pressure, monitoring renal function, or measuring liver enzymes.
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PMID:The hematologic system as a marker of organ dysfunction in sepsis. 1283 83

MDS are a diverse group of primary and secondary bone marrow disorders that are characterized by cytopenias in blood, prominent dysplastic features in blood or bone marrow, and normal or hypercellular bone marrow. MDS in cats are typically associated with FeLV infection. Dogs with MDS-RC and MDS-Er seem to respond to erythropoietin administration and have prolonged survival. Dogs with MDS-EB respond poorly to present treatments, and survival is short. Prognosis and probability of progression to acute myelogenous leukemia can be predicted based on the percentage of myeloblasts in bone marrow. Several experimental therapeutic modalities in human beings have been described that may be useful in treating MDS-EB in dogs and cats. Aplastic pancytopenia is a relatively rare disorder in dogs and cats. Causes include Ehrlichia spp, Parvovirus, and FeLV infections; sepsis; chronic renal failure; drug and toxin exposure; and idiopathic causes. Diagnosis is based on identification of multiple cytopenias in the blood and hypoplastic/aplastic bone marrow, with the marrow space replaced by adipose tissue. Treatment and outcome are dependent on determining the underlying cause of the bone marrow failure.
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PMID:New insights into the physiology and treatment of acquired myelodysplastic syndromes and aplastic pancytopenia. 1466 1

Many advances have improved the care of critically ill patients, but only a few have been through the use of pharmaceutical agents. Recently, the US Food and Drug Administration (FDA) approved drotrecogin alfa (activated), or recombinant human activated protein C, for the treatment of patients with a high risk of death from severe sepsis. Drotrecogin alfa (activated) has antiinflammatory, antithrombotic and fibrinolytic properties. When given as a continuous intravenous infusion, recombinant human activated protein C decreases absolute mortality of severely septic patients by 6.1%, resulting in a 19.4% relative reduction in mortality. The absolute reduction in mortality increases to 13% if the population treated is restricted to patients with an APACHE II score greater than 24, as suggested by the FDA. The most frequent and serious side effect is bleeding. Severe bleeds increased from 2% in patients given placebo to 3.5% in patients receiving drotrecogin alfa (activated). The risk of bleeding was only increased during the actual infusion time of the drug, and the bleeding risk returned to placebo levels 24 hours after the infusion was discontinued. Patients treated in the intensive care unit frequently develop anemia, usually severe enough to require at least one transfusion of red blood cells. With the recent discovery of the harmful effects of allogeneic red blood cell transfusions and the increasing shortage of available red blood cell products, emphasis has been placed on minimizing transfusions. Patients who receive exogenous recombinant human erythropoietin maintain higher hemoglobin levels, in spite of requiring fewer transfusions during their stay in the intensive care unit. Recombinant human erythropoietin appears to be effective whether it is given as 300 units/kg of body weight subcutaneously every other day or as 40,000 units subcutaneously every week. Differences in hemoglobin values were not apparent until at least one week of therapy, but they continued to diverge after that initial week. Furthermore, the incidence of adverse events was similar to that of patients receiving placebo and there was no difference in mortality, suggesting that avoidance of blood transfusions did not translate into increased survival. Thus, recombinant human erythropoietin appears to be both safe and effective in treating the anemia found in critically ill patients, but it is less clear that such treatment is cost effective, especially in the higher dose regimens. Hypotension in patients with septic shock is often difficult to correct. Despite enormous dosages of catecholamines, many of these patients continue to have inadequate blood pressures. Inadequate levels of vasopressin have been identified in patients with septic shock, as well as in other patients with hypotension secondary to refractory vasodilatation. Vasopressin is a peptide hormone secreted from the posterior pituitary in response to hyperosmolality, hypovolemia or hypotension. Levels of vasopressin initially rise in patients with septic shock, but as hypotension persists, vasopressin levels fall below normal. Administration of exogenous vasopressin in physiologic dosages significantly increases blood pressure in patients with shock associated with sepsis and other vasodilatory states. This rise in blood pressure is often significant enough that endogenous catecholamines can be decreased and frequently discontinued entirely. Early withdrawal of the vasopressin replacement infusion results in recurrent hypotension. Unfortunately, randomized, blinded, placebo-controlled trials showing improvement in long-term outcomes such as mortality and length of stay are still lacking.
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PMID:New additions to the intensive care armamentarium. 1504 37

Anemia may be the most common illness of critically ill patients. The majority of critically ill patients are anemic at admission to the intensive care unit (ICU), and hemoglobin concentrations typically decline during the first 3 days of ICU stay. Hemoglobin continues to decline for patients with sepsis and higher severity of illness. This patient population may be at particular risk of adverse consequences of anemia given the cardiovascular, respiratory, and metabolic compromise frequently encountered during critical illness. The etiology of anemia of critical illness is multifactorial, resulting from phlebotomy, gastrointestinal bleeding, coagulation disorders, blood loss from vascular procedures, renal failure, nutritional deficiencies,bone marrow suppression, and impaired erythropoietin response.
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PMID:Blood conservation for critically ill patients. 1513 68

Apoptosis of lymphoid tissues during sepsis is well documented and linked to the pathobiology of organ failure and death. In this study, we evaluated the effect of a single dose of recombinant erythropoietin (EPO) on thymic and splenic apoptosis in an endotoxic sepsis model. Young male Wistar rats were divided into 3 groups and administered intraperitoneally (IP) either normal saline; lipopolysaccharide (LPS) 10 mg/kg; or EPO (5000 U/kg) 30 min before lipopolysaccharide. Six hours following LPS administration animals were sacrificed. Apoptosis was assessed by hematoxylin-eosin staining, terminal deoxynucleotide transferase-mediated fluorescein-dUTP nick end labeling (TUNEL), and caspase-3 immunostaining. When compared with animals given LPS, animals pretreated with EPO displayed reduced splenic and thymic TUNEL positivity of 44+/-3 (p<0.05) and 143+/-4 (p<0.05) nuclei per high power field (hpf), respectively. Caspase-3 positivity was also significantly reduced in the spleen and thymus, with 31+/-4 (p<0.05) and 93+/-3 (p<0.05) positive stained nuclei per hpf, respectively. Serum nitrite levels were elevated in animals given lipopolysaccharide. Pretreatment with EPO attenuated the increase in nitrite levels; however, this did not reach statistical significance. We conclude that a single dose of recombinant erythropoietin can reduce thymic and splenic apoptosis associated with lipopolysaccharide administration.
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PMID:Erythropoietin attenuates lipopolysaccharide-induced splenic and thymic apoptosis in rats. 1608 14

Erythropoietin is a glycoprotein hormone mainly released by the kidney, which stimulates red blood cell production. However, in sepsis, the mechanisms responsible for the final increase in circulating erythropoietin remain unclear Seventeen critically ill patients with Simplified Acute Physiologic Score average 66 (range 43 to 103) were included in this study. Ten patients survived and seven died within 28 days. Blood samples obtained at different times were assayed for erythropoietin, cytokine levels and lactate measurements. PCO2 gap was assessed to detect the presence of gastric mucosal acidosis. Erythropoietin decreased in the patients who survived while it remained high or increased in non-survivors (37+/-6.5 vs 147+/-6. 7 UI/l respectively, P<0.05). Erythropoietin plasma levels were correlated with IL-6 levels (r=0.84, P<0.05) and TNFalpha levels (r=0.84, P<0.05). We observed a significant positive relationship between erythropoietin plasma levels and lactate concentrations (r= 0.89, P< 0. 05) and with PCO2 gap (r=0.9, P < 0.05). No correlation was found between erythropoietin concentration and the other parameters. High serum erythropoietin levels in non-survivors were observed with septic shock despite an increase in the levels of proinflammatory cytokines. We found a relationship between erythropoietin concentration and biological markers of tissue hypoperfusion i.e. lactate levels or PCO2 gap. This relationship could suggest tissue hypoperfusion as the stimulating factor for erythropoietin production in septic shock.
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PMID:Serum erythropoietin levels in septic shock. 1623 74

Thrombopoietin (TPO) and its receptor (TPOR) are expressed in the central nervous system (CNS). Although TPO shares significant homology with various neurotrophins, recent data indicate a proapoptotic function of TPO in the CNS. In this study, TPO concentrations were analyzed in the cerebrospinal fluid (CSF) of neonates. Human neuroblastoma-derived SH-SY5Y cells were established to elucidate the effects of inflammation and hypoxia on neuronal Tpo expression. TPO was detectable in the CSF of 6 of 15 neonates with bacterial infection/sepsis (median 140, range 2-613 pg/mL), 5 of 9 neonates with posthemorrhagic hydrocephalus (median 31, range 1.4-469 pg/mL), 3 of 4 neonates with posthemorrhagic hydrocephalus plus bacterial infection/sepsis or meningitis (median 97, range 6-397 pg/mL), but not in controls ( n = 3). Neither the presence of detectable TPO nor its level in the CSF significantly correlated with any clinical or laboratory parameter. In SH-SY5Y cells, TPO and TPOR expression was detected by RT-PCR and Western blot analysis. In vitro, interleukin-6 (IL-6) did not significantly change Tpo gene expression. In contrast, Tpo mRNA expression significantly decreased under hypoxia, whereas erythropoietin (EPO) mRNA expression increased. In conclusion, our data provide evidence that in neuronal cells, TPO production is regulated by different mechanisms than in hepatocytes.
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PMID:High thrombopoietin concentrations in the cerebrospinal fluid of neonates with sepsis and intraventricular hemorrhage may contribute to brain damage. 1731 41


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