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

A 46 year old female was admitted to our emergency room because of cardiopulmonary arrest by hanging. After ten minutes cardiopulmonary resuscitation, she was resuscitated but her consciousness did'nt recover. CT-scans on the day of admission showed no abnormalities but on the second hospital day it showed symmetrical low density areas within the basal ganglia, the thalamus, the hippocampus, and the occipital lobe. There were marked enhanced effect in cerebral sulci due to cytotoxic edema of hypoxic encephalopathy. She was comatose for a week, her pupils were dilated, light reflex and other brain stem reflex were absent. CT-scans on the sixth hospital day showed marked brain swelling with disappearance of the ventricular systems (so called brain tamponade). Brain death was confirmed on the basis of Japanese Criteria on the seventh and tenth day of admission. She had been suffering from pneumonia and urinary tract infection with an elevation of temperature since the fourth hospital day. We detected Enterobacter Cloacae (E. Cloacae), Klebsiella Oxytoca from the cultures of sputum and urine. On the tenth hospital day her temperature was running up to 39.4 degrees C and blood count revealed a peripheral blood leucocytosis of 40,300/mm3 with a shift to the left. E. Cloacae was also detected from the cultures of blood. Skull roentgenogram showed multiple gas collections in the ventricular systems. CT-scans on the fourteenth hospital day showed multiple gas-containing brain abscess. The etiology of this infection was considered due to septicemia of E. Cloacae. She died from acute renal failure on the fifteenth hospital day. Consent for autopsy was not accepted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Non-clostridial gas-producing brain abscess in a brain death patient--report of a case]. 329 38

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

In a five-year retrospective study, there were 57 episodes of bacteremia among 1623 admissions (3.5%) of patients suffering from cirrhosis. Gram-positive bacteria were found in 70% of the episodes, gram-negative bacteria in 30%. All of the gram-positive bacteria found were fully sensitive to methicillin and to gentamicin. The gram-negative bacteria found were all sensitive to gentamicin, but only 50% were sensitive to ampicillin. The distribution between gram-positive and gram-negative bacteria was the same, irrespective of whether the patients acquired the infection inside or outside the hospital. More than 50% of the patients suffered from one or more of the following complications of cirrhosis: ascites, encephalopathy and haematemesis. Twenty-one patients died within seven days after the bacteremia was diagnosed. Bacteremia is a serious complication of advanced cirrhosis, and it is recommended that adequate antibiotic treatment is started when septicemia is suspected.
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PMID:Bacteremia in patients suffering from cirrhosis. 371 May 95

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

Sepsis and critical illness occur as complications of illness, injury, or surgery in approximately 5% of patients in our critical care unit. Clinical evaluation of the nervous system is difficult in this clinical setting, and electrophysiologic studies are therefore quite valuable. Electroencephalography detects encephalopathy and electromyography (EMG) and nerve conduction studies detect neuromuscular disorders at early stages of their development. Thus, septic encephalopathy occurs in almost all patients and critically ill polyneuropathy in at least 50% of such patients. The polyneuropathy is a predominantly distal axonal degeneration of motor and sensory fibers. A catabolic myopathy is also present, but is difficult to detect electrophysiologically. No defect in neuromuscular transmission has so far been demonstrated. Both the encephalopathy and polyneuropathy may be quite severe, but with vigorous management of the sepsis and critical illness complete recovery may occur in the 40% of patients who survive.
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PMID:Electrophysiologic studies of critically ill patients. 382 86

Acute hepatic failure is characterized by a sudden catastrophic compromise of hepatic failure that causes clinical signs such as anorexia, depression, vomiting, diarrhea, icterus, and encephalopathy. Injurious hepatotoxins, drugs, infectious agents, or metabolic disturbances can cause acute hepatic failure; however, in many cases, the inciting cause is not determined. Treatment is aimed at controlling complications such as fluid-electrolyte imbalances, hepatic encephalopathy, hypoglycemia, bleeding diathesis, gastric ulcer, sepsis, and endotoxemia, in order to provide time for liver regeneration and recovery.
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PMID:Acute hepatic failure. 387 99

From 1974 through 1982, fulminant hepatitis was diagnosed in 34 patients at our institution. Of these patients, only two survived (survival rate, 6%). This syndrome was caused by viruses (B and non-B hepatitis and herpes simplex) in 23 patients, hepatotoxic drug in 6, Wilson's disease (hepatolenticular degeneration) in 3, and industrial poisons in 2. Most of the patients died within 10 days after the onset of encephalopathy. The poor prognosis in our group of patients was probably related to the preponderance of older patients and cases caused by non-B hepatitis virus. In our patients, the clinical course was complicated by renal failure, ascites, bleeding, sepsis, pancreatitis, and seizures. The major cause of death was hepatic failure.
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PMID:Fulminant hepatitis: Mayo Clinic experience with 34 cases. 392 80


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