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

Between March 1982 and September 1983, 40 inpatients (25 men and 15 women, mean age 53 years) with alcoholic cirrhosis and total serum bilirubin greater than or equal to 5 mg per dl were studied. Those with hepatocellular carcinoma, renal failure, hyponatremia, septicemia, spontaneous bacterial peritonitis, gastrointestinal bleeding, and hepatic coma were excluded. Patients were studied for 28 days. The two groups were offered an oral diet containing 40 kcal per kg per day. Patients in the supplementary parenteral nutrition group received 40 kcal per kg per day and 200 mg nitrogen per kg per day using a central catheter. The major endpoint was total serum bilirubin on Day 28. On admission, serum bilirubin was not significantly different in the two groups: oral group, 12.5 +/- 6.6 mg per dl; supplementary parenteral nutrition group, 12.3 +/- 8.5 mg per dl. On Day 28, serum bilirubin was lower in the supplementary parenteral nutrition group (2.5 +/- 1.4 mg per dl) than in the oral group (4.1 +/- 2.2 mg per dl) (p less than 0.02). Serum bilirubin was also lower in the supplementary parenteral nutrition group than in the oral group on Days 7, 14 and 21 (p less than 0.05). Analysis of covariance, considering serum bilirubin on admission and at randomization and time between admission and randomization, confirmed these results. On Day 28, anthropometric parameters, serum transferrin, prealbumin and retinol-binding protein were higher in the supplementary parenteral nutrition group, but the differences were not significant. Serum albumin was significantly lower in the supplementary parenteral nutrition group. The incidence of encephalopathy and sepsis was not significantly different between the two groups.
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PMID:A randomized clinical trial of supplementary parenteral nutrition in jaundiced alcoholic cirrhotic patients. 308 33

We describe our experience in the treatment of acute liver failure in 620 patients who developed grade 3 or 4 encephalopathy between 1973 and June 1985. The principal aetiologies were paracetamol-induced hepatic necrosis, viral hepatitis, halothane hepatitis and idiosyncratic drug reactions. Cerebral oedema is a major cause of death in these patients and is most effectively treated with mannitol (20%). Renal failure occurs in between 30% and 75% of cases, depending on aetiology, and is most effectively managed by haemodialysis. Electrolyte and acid-base abnormalities are common. Haemodynamic abnormalities encountered include a high cardiac output, low peripheral vascular resistance, hypotension and venodilatation. Assisted mechanical ventilation is frequently required to treat hypoxia caused by pneumonia, atelectasis, haemorrhage and oedema. A coagulopathy is always present but coagulation factors and platelets are given only when the patient is clinically bleeding. These patients are prone to sepsis and this is a significant cause of death. Hypoglycaemia is common and must be actively and frequently sought. The use of charcoal haemoperfusion has been associated with improved survival, especially when it is started during the grade 3 phase of encephalopathy. Recently survival figures of between 47% and 60% have been achieved for patients with paracetamol-induced liver failure and hepatitis A and B. However the figure for non A non B hepatitis and halothane- and drug-induced liver failure are disappointing at around 15% and liver transplantation is being explored as a treatment option in these patients.
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PMID:Management of acute liver failure. 308 71

The diagnosis of acute viral hepatitis is based on a thorough history (with a detailed review of possible modes of transmission), consistent physical findings (in which stigmata of chronic liver disease are absent), and laboratory tests confirming the presence of acute hepatocyte damage. Specific etiologic entities can be identified by serologic testing. In some cases, infection by more than one hepatitis virus may be revealed. The occurrence of HBV/HDV coinfection may lead to typical, uncomplicated acute hepatitis. In some patients, however, the development of a prolonged prothrombin time and encephalopathy indicates the presence of fulminant disease. The management of patients with such disease usually requires admission to an intensive care unit in order to increase the likelihood that complications will be recognized at an early stage, when intervention might make a difference. Standard interventions include vigorous treatment of hypoglycemia, attention to electrolyte and acid-base disturbances, and antibiotic therapy for bacterial sepsis. Despite aggressive management by experienced teams, fatality rates remain exceedingly high: As many as 75% to 100% of patients with severe encephalopathy die. Liver transplantation has been attempted in a number of cases. Its role remains ambiguous. Survival rates of 50% to 60% have been reported, but selection bias may turn out to have contributed to this apparently favorable outcome. In the patient under discussion, results of a follow-up physical two months after discharge were entirely normal. Liver chemistries were within normal limits, but a test for HBsAg was still positive. During the course of the examination, the patient admitted to having accidentally pricked his skin nearly two months before the onset of his illness while holding a needle that a friend had used for the intravenous injection of heroin. One year later, HBsAg was no longer detectable, but tests for anti-HBc and anti-HBs were both positive. The anti-HBc positivity was attributable to IgG rather than IgG anti-HBc. A test for anti-HDV was negative.
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PMID:Fulminant hepatitis due to HBV/HDV coinfection. 311 12

Between 1976 and 1984, 136 patients with portal hypertension due to extrahepatic obstruction were operated on. Twenty two patients had emergency and 114 elective operations. The operative mortality was 9% and 1%, respectively. Altogether 117 patients (86%) were followed up for from two to 10 years: 17 rebled, none developed encephalopathy or sepsis after splenectomy, and 90% and 75% were alive at five and 10 years respectively. Unlike endoscopic sclerotherapy and treatment with propranolol, operative treatment of variceal bleeding can usually be completed during one admission and carries a low mortality and a fairly low morbidity. Operation seems to be the best form of treatment for poor patients living far from medical facilities in developing countries and may be the treatment of choice in developed countries as well.
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PMID:Operations for portal hypertension due to extrahepatic obstruction: results and 10 year follow up. 312 Sep 6

The pathophysiological changes occurring with increasing grade of encephalopathy were examined in 93 consecutive episodes in 44 patients with liver cirrhosis (37 posthepatic). The incidence of gastrointestinal bleeding and leukocytosis increased significantly when the grade advanced from 1 to 5. The following variables showed a trend for change that did not reach statistical significance: rising serum bilirubin, SGOT, and BUN levels; decreasing serum sodium and chloride levels; and increased incidence of infection. The mean values of the following variables were significantly different in 25 fatal episodes and 68 survivors, implicating a bad prognosis: high serum bilirubin, alkaline phosphatase, and BUN levels; low serum albumin, sodium, and chloride levels; and a higher incidence of severe infections (sepsis, infected ascitic fluid). Because increasing grade of encephalopathy is the most important factor in determining the prognosis of hepatic encephalopathy (mortality 0, 10, 5, 19, and 85 percent in grades 1 to 5, respectively), more efforts should be made to understand and prevent the pathophysiological changes associated with advancing grades of encephalopathy.
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PMID:Pathophysiological changes associated with increasing grade of hepatic encephalopathy. 324 14

In order to determine whether disturbances in GABA homeostasis might play a role in the pathogenesis of sepsis-related encephalopathy, serum and brain tissue GABA concentrations from six areas of the brain (cortex, diencephalon, striatum, hippocampus, midbrain, and pons-medulla) were determined in a rat model of bacterial sepsis (cecal ligation and perforation). The results were compared to those obtained from sham operated control animals. All septic animals demonstrated clinical signs of encephalopathy and had elevated serum GABA levels (0.92 +/- 0.3 uM versus 0.48 +/- 0.15 in controls, p less than 0.01). GABA content in the specific subcompartments of the brain, however, were similar in the two groups. These results indicate that although serum GABA levels are elevated during sepsis, GABA is unlikely to play an important role in the pathogenesis of sepsis-related encephalopathy.
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PMID:gamma-Aminobutyric acid (GABA) and sepsis-related encephalopathy. 334 57

Sixty-four (48%) of 133 children with hematologic malignancy who were admitted to three pediatric ICUs died. Children who required management because of airway obstruction or after general anesthesia had the best outlook (mortality rate of 7% or less); those children who required major circulatory support or mechanical ventilation for hypoxemia did poorly (mortality rate of 84% or greater). Certain conditions in children with hematologic malignancy that require intensive care are associated with a mortality rate of approximately 75%. These include the following: suspected sepsis, interstitial pneumonitis, encephalopathy due to sepsis or hemorrhage. In children with these life-threatening conditions, therapy must be improved because at this stage, the patients do not benefit from admission to the ICU.
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PMID:Outcome of children with hematologic malignancy who are admitted to an intensive care unit. 275 88

Of 26 patients with pheochromocytoma treated between 1974 and 1986, two presented with pheochromocytoma crisis. This unusual presentation consists of hyper- and/or hypotension, high fevers (greater than 40 degrees C), encephalopathy, and multiple organ system failure. Both patients had large tumors associated with markedly elevated levels of epinephrine. Although hypertension was adequately controlled in both patients with phenoxybenzamine, phentolamine (1 patient) and nitroprusside, both patients deteriorated rapidly. The first patient expired during attempts to identify a source of sepsis. None was found at autopsy. The second patient underwent urgent adrenalectomy which reversed the multiple organ system failure and resulted in patient survival. We conclude from review of these patients and three others in the literature that (a) crisis is an unusual presentation of pheochromocytoma; (b) its manifestations include vascular lability, high fever, encephalopathy and multiple organ system failure; (c) it may be the result of increased epinephrine secretion; (d) successful treatment of pheochromocytoma crisis demands prompt diagnosis, vigorous medical therapy and emergent tumor removal if the patient continues to deteriorate.
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PMID:Pheochromocytoma crisis. 341 97

A series of patients with meningococcal infections have been studied and divided in two groups: Group I patients with meningococcal sepsis and group II, those with meningococcal meningitis. Patients in group I presented with more severe encephalopathy, shock, DIC and acute systemic complications. Both groups showed a marked hypoaminoacidemia compared with normal controls (other than for the sulfur containing amino acids and phenylalanine). The concentration of aromatic and basic amino acids, the phenylalanine/tyrosine ratio, the transaminase levels and the negative nitrogen balance were higher in group I patients. The ratio of branched chain to aromatic amino acids was lower in group I. All these differences were statistically significant. The close association between the metabolic derangements and clinical manifestations may help in the understanding of several physiopathological aspects of meningococcal infections.
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PMID:Significance of the changes in plasma amino-acid levels in meningococcal infection. 365 98

Endotoxemia without sepsis was detected with a chromogenic Limulus assay in 36 of 39 (92.3%) cirrhotic patients and was absent in seven healthy volunteers. In 11 patients who underwent elective portasystemic shunt, portal vein endotoxemia was higher than inferior vena caval: p less than 0.05, systemic endotoxin levels did not change, compared to preoperative levels, on the 1st, 2nd, and 3rd postoperative days, attendant to an uneventful recovery. In 21 patients in hepatic encephalopathy after esophagogastric hemorrhage, systemic endotoxemia was higher than in well-compensated cirrhotics: p less than 0.001; it was higher in deep than in light coma: p less than 0.05; it was higher in those who died than in those who survived: p less than 0.001. Endotoxin levels showed a positive correlation with serum bilirubin: r = 0.59, p less than 0.001, and a negative correlation with prothrombin activity: r = -0.59, p less than 0.001. These data show endotoxemia without sepsis is a constant finding in cirrhosis and increasing levels of endotoxemia are associated with hepatic failure, encephalopathy, and death.
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PMID:Endotoxemia, encephalopathy, and mortality in cirrhotic patients. 379 74


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