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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Falciparum malaria remains a major killer in developing countries, particularly for African children. The sequestration of parasitized erythrocytes in the deep microvasculature is mostly mediated by their cytoadherence to activated endothelium. Proinflammatory cytokines and particularly tumor necrosis factor contribute to severe disease but the pathophysiology of coma remains poorly understood. In young children, features of severe malaria include severe anemia, hypoglycemia and cerebral malaria. Half of the children with neurological impairment actually have raised intracranial pressure, and seizures are extremely common. Clinical respiratory distress usually reflects severe lactic acidosis. In non immune adults, pictures of severe sepsis with shock, acute renal failure and respiratory distress syndrome are common and often associated with bacterial coinfection. Although chemotherapy of malaria is challenged by the continuing evolution of antimalarial resistance, quinine remains the first-line drug for severe disease. The optimization of symptomatic management of severe malaria remains a major concern in developing countries.
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PMID:[Severe malaria]. 978 Oct 74

Under normal circumstances, O 2 transport (TO 2 = cardiac output x arterial O 2 content) is regulated to provide sufficient O 2 to meet the demands of oxidative phosphorylation, quantified as the O 2 consumption (VO 2). When metabolic demands increase, TO 2 is augmented and in addition, the fractional extraction of the delivered O 2 by the tissues, the O 2ER, also increases, to levels as high as 0.80 at maximum VO 2. If TO 2 is decreased, at least in the experimental animal, VO 2 can be maintained initially by an increase in O 2ER, but eventually this mechanism is exhausted, VO 2 begins to fall, and the body invokes anaerobic means of energy generation to maintain cell integrity. In normal man, this critical level of TO 2 (TO 2crit) has not been determined, but in experimental animals it has been found once the O 2ER exceeds 0.50. Patients with sepsis and the adult respiratory distress syndrome have a very high mortality and usually die as a result of multiple organ failure. They have in addition, an apparent abnormality in their ability to extract and utilize the delivered O 2. Despite a TO 2 which is often higher than normal, patients with sepsis commonly have a lactic acidosis and when TO 2 is reduced, both groups of patients are usually unable to increase their O 2ER above the normal resting value of 0.33.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxygen delivery and utilization. 1014 15

Metabolic acidosis occurs frequently in small children. The most common causes are hypoxia, sepsis, gastroenteritis and hypovolaemia. Calculation of the anion gap is useful in establishing the cause. An increased anion gap represents unmeasured anions, e.g. lactate in lactic acidosis. Metabolic acidosis was diagnosed in two boys aged one year and six weeks respectively. The first patient had a normal, the second an increased anion gap in blood. By determining the pH and the anion gap in urine it is possible to distinguish between a proximal and a distal tubular disease. The first patient had distal renal tubular acidosis; he recovered after correction of the acidosis. The second patient had a defect in the mitochondrial respiratory chain; he died at the age of seven months.
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PMID:[Metabolic acidosis in children: the usefulness of 'anion gap']. 1032 Dec 98

Physiologic hyperlactatemia must be distinguished from lactate acidosis (lactate > 5 mM/L, pH < 7.32). Sustained lactic acidosis, or changes in lactate in response to inotropic support, are useful predictors of mortality in severe sepsis and trauma, and superior to hemodynamic markers such as DO2 and VO2. Base deficit is a readily available surrogate for plasma lactate, and the addition of gastric tonometry enhances its predictive ability.
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PMID:Lactate in sepsis and trauma--hindrance or help? 1035 4

While there is clear support for the use of continuous renal replacement therapy (CRRT) in critically ill acute renal failure patients, there are other illnesses without renal involvement where CRRT might be of value. These include sepsis and other inflammatory syndromes such as acute respiratory distress syndrome (ARDS) and cardiopulmonary bypass where removal of inflammatory mediators by hemofiltration is hypothesized to improve outcome. Adsorption appears to be the predominant mechanism of mediator elimination. However, the observed hemodynamic improvement can, at least partially, be attributed to a reduction of body temperature or to fluid removal, and the evidence for a clinically important removal of proinflammatory cytokines remains limited. Continuous and therefore smooth fluid removal may improve organ function in ARDS, after surgery with cardiopulmonary bypass, and in patients with refractory congestive heart failure. Continuous removal of endogenous toxins, eventually combined with intermittent hemodialysis, is probably beneficial in inborn errors of metabolism, severe lactic acidosis, or tumor lysis syndrome.
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PMID:Non-renal indications for continuous renal replacement therapy. 1056 Aug 14

Type "B" lactic acidosis has been described in patients receiving the nucleoside analogs zidovudine, didanosine, and fialuridine. Lactic acidosis has also been described in 4 patients receiving combination therapy with stavudine and lamivudine. We describe the development of chronic type "B" lactic acidosis in 3 patients receiving stavudine as a single agent and in 2 patients receiving combination therapy with stavudine and either lamivudine or delavirdine, a nonnucleoside analog. All patients presented with abdominal pain, vomiting, and hepatic steatosis. Other signs of mitochondrial toxicity included pancreatitis and myopathy (2 cases). The mean duration of stavudine therapy was 9.4 months, and the mean observed peak lactate level+/-SD was 10.3+/-5 mmol/L. After discontinuation of stavudine treatment, lactic acidosis improved in 4 patients after 4-60 weeks, and 1 patient died. Evaluations for other causes of lactic acidosis, including hypoxemia, malignancy, sepsis, and cardiogenic shock, were negative.
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PMID:Lactic acidosis associated with stavudine administration: a report of five cases. 1061 55

In septic shock, the extent to which lactic acidosis (LA) is a consequence of splanchnic lactate overproduction (SLP) or impaired hepatic lactate extraction (HLE) is not clear. We examined SLP and HLE in E. coli sepsis in dogs. We further determined the effects of vasopressor treatments, which included phenylephrine, dopamine, norepinephrine, and a combination of dobutamine and norepinephrine treatment, on SLP and HLE in respective groups. The animals were studied while anesthetized and ventilated. During sepsis, SLP increased as compared with presepsis (-0.017 versus 0.07 mmol/min, p < 0.05), but this increase could not be explained by reduced splanchnic oxygen delivery (SOD). During sepsis, HLE increased as compared with baseline (0.8 versus 8%, p < 0.05), but was significantly lower than that found during lactic acid loading in nonseptic dogs. None of the vasopressor treatments had a detrimental effect on SLP. These results indicate that LA in sepsis occurs secondary to an increase in splanchnic lactate production that is not related to reduced splanchnic oxygen delivery, as well as to a decrease in hepatic lactate extraction. Effects of different vasoactive agents did not alter either splanchnic lactate production or hepatic lactate extraction in this sepsis model.
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PMID:Impaired hepatic extraction and increased splanchnic production contribute to lactic acidosis in canine sepsis. 1067 95

A patient with cholangiocarcinoma, metastatic to the liver and lungs, developed acute fulminant lactic acidosis in the absence of overt hepatic failure, sepsis, hypoxia, or circulatory failure. Despite extensive tumor replacement of hepatic parenchyma, no acid-base disorder was present during initial evaluation. The onset of acute lactic acidosis was temporally associated with the development of otherwise asymptomatic episodes of intermittent atrial arrhythmias. Once established, lactic acidosis was inexorably progressive, despite resolution of arrhythmias. Extensive areas of acute necrosis within the large hepatic metastases were demonstrated on postmortem examination, suggesting that local tissue ischemia, precipitated by cardiac arrhythmias, lead to excessive lactic acid production.
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PMID:Acute fulminant lactic acidosis complicating metastatic cholangiocarcinoma. 1069 99

Pentoxifylline is a phosphodiesterase inhibitor, known to suppress tumour necrosis factor-alpha production and improve cardiopulmonary parameters and survival in animal models of sepsis. Using a porcine model of abdominal trauma resulting from the combined insults of haemorrhage and infection, a randomised placebo-controlled trial was conducted of pentoxifylline (20 mg/kg bolus followed by 20 mg/kg infusion over 1 h) administered in addition to a colloid resuscitation regimen. Female Large White pigs (45-60 kg) were bled 40% of their blood volume and peritonitis was induced using E. coli (O18: K1: H7) in an autoclaved faecal suspension. Animals were resuscitated with either colloid alone (n=5) or colloid plus pentoxifylline (n=5). Pentoxifylline attenuated increases in mean arterial and pulmonary artery pressures and reduced both systemic and pulmonary vascular resistance. It worsened the lactic acidosis associated with 'septic shock' and failed to reduce serum TNF-alpha levels. Pentoxifylline, in the high doses used in this study, does not have a role as an adjunct to resuscitation in this clinically relevant model of trauma.
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PMID:Pentoxifylline fails to improve organ dysfunction and survival when used in the resuscitation of a porcine model of haemorrhage and abdominal sepsis. 1069 1

Placental tumors are rare in pregnancy. They cause nonspecific complications such as polyhydramnios, fetal anemia, fetal thrombocytopenia and cardiac decompensation with non-immunological hydrops fetalis. In the presented case a very large placental hemangioma was connected with polyhydramnios, premature delivery, fetal anemia and thrombocytopenia, maternal serum alpha fetoprotein elevation and congenital lactic acidosis. After delivery a severe state of the newborn was caused by oligovolemic shock. In the course of the disease the neonatal state steadily deteriorated mainly because of sepsis, cerebral hemorrhage and metabolic acidosis despite adequate therapy. The organic acids assessment in the blood serum of a newborn child showed a very strong signal of lactic acid and an increase in parahydroksyfenylolactic acid. Postmortal examination confirmed prematurity, respiratory distress syndrome, sepsis and cerebral hemorrhage. These symptoms probably resulted from the presence of a placental tumor of considerable size of 12 cm and congenital lactic acidosis, which to our knowledge, have not been described in the available literature until now. In conclusion it should be underlined, that there exists difficult to explain relationship between the presence of a placental haemangioma and severe metabolic changes resulting in high mortality and morbidity of the newborn.
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PMID:[Giant placental angioma with polyhydramnios, high level of alpha-fetoprotein and neonatal congenital lactic acidosis]. 1071 13


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