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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with liver cirrhosis and ascites suffer from spontaneous bacterial peritonitis (SBP) in up to 25%. The typical clinical signs are abdominal pain with tenderness and fever. 30% have no signs of peritonitis. Then clinical worsening, encephalopathy, rising serum creatinine levels, and therapy resistant ascites may be the only clinical features. SBP must be differentiated from bacterascites and culture negative neutrocytic ascites by the polymorphonuclear neutrophil (PMN) count in the ascites and the presence of positive culture results, which has prognostic implications. Gram negative rods from the colon play an important etiological role in SBP. Gastrointestinal bleeding, lack of serum complement, a low ascites protein and the extent of intrahepatic shunts predispose to SBP. Then, prophylaxis with the comparable drugs neomycin and norfloxacin is indicated. Coexisting encephalopathy has to be treated by the therefore effective neomycin. Otherwise, norfloxacin is the drug of choice because of better acceptance and lower costs. Chemical parameters of the ascites (pH value less than 7.4; LDH and lactate greater than serum levels; glucose less than 50 mg%) help to assess the severity of peritonitis. The course of ascitic PMN under therapy and the time of persisting positive cultures can discriminate SBP from secondary peritonitis. Antibiotics of choice are amoxicillin-clavulanic acid and cefotaxime. Short course therapy (5 days) is a effective as long course therapy (10 days). Today SBP is no more life-threatening because diagnosis, prophylaxis and therapy have improved. However, complication rate of patients with liver cirrhosis and ascites has not changed.
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PMID:[Spontaneous bacterial peritonitis]. 141 38

Advanced hepatic injury can be identified by the appearance of jaundice, coagulopathy, or encephalopathy but these conditions are late, irreversible findings and represent the end stage of a long insidious process. Currently available methods for assessing "liver function" (SGOT, SGPT, GGT, LDH, etc.) do not actually measure liver function. In this study we prospectively evaluated "true" liver function in patients undergoing porto-systemic shunt. Effective hepatic blood flow [low dose galactose clearance (EHBF)], hepatocyte transport (theophylline levels at 24 hr), and hepatic conjugation ability [acetaminophen metabolism to its glucuronide and sulfate conjugates ( (S + G)/A) and acetaminophen remaining at 24 hr (A24)] were measured in normal males (NL) and in patients pre- and post-8-mm H-graft portacaval shunt (PCS). All data are means +/- SEM, analyzed by Student's t test, and significance was accepted if P less than 0.05. There were no significant differences in EHBF even after PCS. Hepatocyte transport was decreased in pre-op (1.43 +/- 0.16 vs 0.74 +/- 0.08) and post-op (1.79 +/- 0.34) PCS patients. Hepatic conjugating ability was also decreased in pre-op PCS patients [A24 was increased (0.24 +/- 0.11 vs 0.01 +/- 0.01) while the ratio of conjugation products to acetaminophen remained the same]. The ability of the liver to conjugate substrate was severely compromised postoperatively [A24 - 1.27 +/- 0.67, (S + G)/A - 1.19 +/- 0.34]. We believe that changes in liver function can be accurately measured using these noninvasive methods, and in using these methods we have identified altered hepatocyte transport and conjugating ability in patients undergoing porto-systemic shunt surgery.
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PMID:Hepatic function after porto-systemic shunt. 174 Sep 38

Neurological investigations were performed for 53 cases with chronic lymphocytic thyroiditis diagnosed by pathology and serum antithyroid antibodies determination. Of the 53 cases, 29 had different types and severity with neurological findings, which could be divided into 5 groups: 1) Elevated levels of acetylcholine receptor antibody in 13 cases (24.1%); 2) Myopathy and weakness accompanied by elevated serum enzyme levels (GOT, CPK, LDH and alpha-HBDH) in 7 cases (13%); 3) Peripheral neuropathy in 6 cases (11.1%); 4) Encephalopathy in 2 cases (3.7%); and 5) The changes in sella turcica in 2 cases. Our data showed that the neuropathy was not closely correlated to the duration of chronic lymphocytic thyroiditis and seemed that it had no relation with the thyroid function and titer of antithyroid antibodies. However, neuropathy occurred more often in cases with both chronic lymphocytic thyroiditis and some other autoimmune disorders, suggesting that abnormal immune function might be the common background patients with chronic lymphocytic thyroiditis and neuropathy. The aforementioned data suggest that the hypothyroid function and high titer of antithyroid antibodies might not be a prerequisite for developing neuromyopathies.
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PMID:[Neuropathy and myopathy in patients with chronic lymphocytic thyroiditis]. 214 91

We have suggested that the neuroglycopenia of infective encephalopathy results in increased lactate production in muscle as an alternative cerebral fuel. Two probable mechanisms for enhanced lactate production in infective encephalopathy are fatty acidaemia and increased LDH activity. Hyperglycaemia-producing infusions should then result in clinical and metabolic recovery. Twenty-two children with encepahlopathy were studied over 2 1/2 week periods. There was normoglycaemia at admission together with hyperlactataemia (p less than 0.004), fatty acidaemia (p less than 0.004) and increased serum LDH activity (p less than 0.005). Therapeutic hyperglycaemia resulted in recovery and a progressive return of metabolic aberrations to normality. Two case reports detail the responses to such management.
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PMID:Lactate production in type B hyperlactataemia due to infective encephalopathy. 370 32

The risk for developing acute liver failure after halothane exposition was calculated between 1:8,000 and 1:36,000. The case report given on a 22 year old man with halothane-induced hepatic failure is unusual, because the typical risk factors as age over 40, female sex, obesity, and previous exposure to halothane were not present. Two days after exposure to halothane the patient suffered acute liver failure with severe coagulopathy (factor V = 5% activity), and encephalopathy grade IV complicated by renal failure and respiratory insufficiency. Maximal increases of enzymes in blood were AST 3900 U/L, ALT 2570 U/L, LDH 10600 U/L. After six days the patient underwent liver transplantation with complete anuria and instable circulation. Explanted liver showed massive necrosis (70% of parenchyma) and fatty changes. The liver transplant had immediately a good function and renal failure resolved within three days. In the follow-up of 3 1/2 years the patient suffered no further complications. Culturing the patient's lymphocytes in the lymphocyte transformation test a strong reaction could be detected with a stimulatory index of 20. Maximal proliferation was observed when lymphocytes were incubated with plasma metabolites of a volunteer drawn 120 minutes after anesthesia with halothane was started.
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PMID:[Liver transplantation in halothane-induced liver necrosis]. 802 96

The author reported eleven patients with brainstem edema on cranial CT. Nine had acute encephalopathy or Reye syndrome and the other two had acute encephalitis. Seven cases died and four cases survived. Dead cases showed brainstem edema significantly faster than the survivors. Laboratory examinations revealed significant differences of LDH, platelet and HCO3(-) between the two groups. Six patients died in the winter. The duration of convulsion was more than 30 minutes in all the dead cases.
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PMID:[Brainstem edema in patients with acute encephalopathy and encephalitis]. 978 Jul 39

We studied the clinical and CT findings of 3 children with acute encephalopathy associated with adenovirus type 7 (AD-7) infection. Seizures in all the patients developed from 8 to 10 days after the onset of pyrexia. The values of serum AST, LDH and CRP elevated and those of WBC and serum protein decreased at the onset of encephalopathy. None of the patients had CSF leukocytosis. CT showed mild brain atrophy in all patients. A steroid pulse therapy was effective in one patient. The pathogenesis of encephalopathy is unknown. However, its onset and the success of the steroid pulse therapy suggested that it is a post infectious encephalitis. These findings, as well as the data of blood examination and of previous reports, implicated adverse effects of cytokines in the pathogenesis of this encephalopathy.
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PMID:[Three cases with acute encephalopathy related with adenovirus type 7 infection]. 1065 55

To analyze whether exposure to oxygen-glucose deprivation (OGD) of immature rat brain slices might reproduce the main pathophysiologic events leading to neuronal death in neonatal hypoxic-ischemic encephalopathy (NHIE), 500 microm-thick brain slices were obtained from 7-day-old Wistar rats, and incubated in oxygenated physiological solution. In OGD group, oxygen and glucose were removed from the medium for 10-30 min (n = 25); then, slices were re-incubated in normal medium. In control group the medium composition remained unchanged (CG, n = 30). Medium samples were obtained every 30 min for 3 h. To analyze neuronal damage, slices were stained with Nissl and CA1 area of hippocampus and cortex were observed under microscopy. In addition, neuronal death was quantified as LDH released to the medium determined by spectrophotometry. Additionally, medium glutamate (Glu) levels were determined by HPLC and those of TNFalpha by ELISA, whereas inducible nitric oxide synthase expression was determined by Western blot performed on slices homogenate. Optimal OGD time was established in 20 min. After OGD, a significant decrease in the number of neurones in hippocampus and cortex was observed. LDH release was maximal at 30 min, when it was five-fold greater than in CG. Furthermore, medium Glu concentrations were 200 times greater than CG levels at the end of OGD period. A linear relationship between Glu and LDH release was demonstrated. Finally, 3 h after OGD a significant induction of iNOS as well as an increase in TNFalpha release were observed. In conclusion, OGD appears as a feasible and reproducible in vitro model, leading to a neuronal damage, which is physiopathologically similar to that found in NHIE.
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PMID:Immature rat brain slices exposed to oxygen-glucose deprivation as an in vitro model of neonatal hypoxic-ischemic encephalopathy. 1592 37

The aim of this study was to assess the validity of serum and CSF oxidative status of patients with IE in their initial stage through the d-ROM (Diacron-Reactive Oxygen Metabolites, Italy) test, compared to those with other neurological diseases. The study was conducted on the following four groups: (1) influenza virus-associated encephalopathy (IE, n = 8), including four patients showing neurological sequelae or mortal; (2) influenza virus-associated febrile seizures (IFS, n = 11); (3) febrile convulsion (FC, n = 10): (4) enterovirus-associated encephalopathy (EE, n = 4), including one patient with neurological sequelae. The CSF d-ROM levels in the IE group were significantly higher than those in the IFS and the FC groups but not in the EE group. In addition, general laboratory findings such as leukocytes, platelets, C-reactive protein, aspartate aminotransferase, creatinine, creatinine kinase and LDH, including interleukin-6 (IL-6), were analyzed in each group. The CSF d-ROM levels in the IE group were significantly higher than those in the IFS and FC groups but not in the EE group. As for the serum d-ROM levels and general laboratory findings, with the exception of CSF IL-6 levels in IE, no significant differences were detected compared with the other groups. In patients with IE, the CSF d-ROM levels could be a valid predictive biomarker of the severity, and oxidative stress may be related to the pathogenesis of IE.
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PMID:Diagnostic and predictive value of CSF d-ROM level in influenza virus-associated encephalopathy. 1641 81

Children with sequelae of perinatal hypoxic-ischemic encephalopathy (HIE) occasionally suffer from cytokine-related disease. We investigated 12 children with perinatal HIE sequelae, who died in childhood, concerning (1) the incidence of cytokine-related disease as the cause of death, and (2) the characteristics of the cytokine-related disease. Six (50%) of the 12 patients died from cytokine-related disease:two had virus-associated hemophagocytic syndrome (VAHS) ; one had acute encephalopathy;one had systemic inflammatory response syndrome (SIRS); and two had severe pneumonia/acute respiratory distress syndrome (ARDS). These six patients presented with increased liver transaminase, LDH, and CK, and decreased platelet count and albumin. This study shows the high incidence of cytokine-related disease as the cause of death in children with perinatal HIE sequelae. Further investigation is needed to clarify the pathogenesis of this disease.
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PMID:[High incidence of fatal cytokine-related disease among children with sequelae of perinatal hypoxic-ischemic encephalopathy]. 1709 63


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