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

During the past 32 months, 22 consecutive unselected patients who had bled from oesophageal varices have undergone mesocaval "H" graft operations. There have been nine deaths, three in the early and six in the late postoperative periods. Two deaths were the result of bleeding complicating severe primary fibrinolysis and three were due to disseminated sepsis, one originating from an infected shunt. Continued alcohol intake may have contributed to five of the late deaths. Ten of the 19 patients who left hospital developed some degree of hepatic encephalopathy easily controlled by diet and medical therapy. However, in one case the development of grade IV coma necessitated ligation of the shunt to reverse the coma. Patency of the shunt was demonstrated in all but one patient. Recurrence of bleeding occurred only in this patient and the one in whom the shunt was ligated. Although the operation had a comparatively low operative mortality, the long-term mobidity and mortality were no better than those of the more conventional portacaval anastomosis.
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PMID:The mesocaval "H" graft: experience with 22 cases. 30 Jan 41

Several toxic factors have been implicated in the pathogenesis of hepatic encephalopathy (PSE) among which ammonia plays a dominant role. More recently, the gamma-aminobutyric acid (GABA) hypothesis in which an increase in the GABA-ergic tone and the presence of one or more GABA/benzodiazepine receptor ligands which interact with that receptor, has been proposed. We investigated the levels of GABA and ammonia in plasma of patients with acute PSE to test the hypothesis that elevated plasma GABA levels would be found in acute encephalopathy and that GABA levels would correlate with the degree of hepatic encephalopathy. We measured plasma levels of GABA and ammonia during an acute episode of PSE, spontaneous or precipitated by gastrointestinal bleeding or sepsis, and performed assessments of PSE by the PSE index. Patients were evaluated before and two days after standard treatment with lactulose. We also measured plasma GABA levels in the hepatic vein of a selected group of patients undergoing hemodynamic studies. Plasma GABA levels were significantly higher in patients with acute PSE (458 +/- 108 pmol/mL) when compared with normal subjects (110 +/- 23 pmol/mL) (p < 0.01) although no correlation was found between plasma GABA concentration and the degree of PSE. Changes in plasma ammonia, however, correlated with improvements in the PSE index (r = 0.56; p < 0.02) and with abnormalities in the EEG (r = 0.65; p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Association of plasma ammonia and GABA levels and the degree of hepatic encephalopathy]. 148 27

We elected to test the hypothesis that the metabolic encephalopathy associated with systemic sepsis may have a pathogenesis that is similar to hepatic encepathology, ie, as the consequence of hepatic dysfunction that induces alterations in synthesis of catecholic and noncatecholic neurotransmitters. Eleven patients with septic encephalopathy were compared with nine patients with septic encephalopathy and nine normal controls with respect to blood and cerebrospinal fluid (CSF) amino acid profile, phenylethylamine and its metabolite phenylacetic acid, and blood ammonia. Blood and CSF levels of phenylacetic acid increased markedly in septic and hepatic encephalopathy while CSF phenylethylamine levels were not increased in either condition, presumably due to rapid turnover. The CSF concentrations of all the aromatic amino acids were increased in hepatic encephalopathy, whereas in the patients with sepsis, only phenylalanine levels were increased. Evidence of stimulated neutral amino acid transport into brain was demonstrated in hepatic not septic encephalopathy and appeared to correlate with the CSF glutamine concentration. Blood ammonia levels were increased in hepatic but not in septic encephalopathy. Our data support the hypothesis that metabolites of phenylethylamine contribute to encephalopathy in systemic sepsis and hepatic failure; however, the entities differ in other respects.
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PMID:Septic encephalopathy. Evidence for altered phenylalanine metabolism and comparison with hepatic encephalopathy. 230 19

Patients with sepsis often manifest symptoms of encephalopathy similar to those observed in portasystemic encephalopathy. As a causal relationship has been demonstrated between hepatic encephalopathy and a deranged brain neurotransmitter profile, the catecholaminergic and serotoninergic brain neurotransmitter profile in a septic rat model was investigated. Septic animals exhibited lower levels of norepinephrine (NE), 3,4-dihydroxyphenylacetic acid, and homovanillic acid compared to normal controls. Severely septic animals with encephalopathy exhibited significantly lower levels of NE, dopamine, 5-hydroxytryptamine, and 5-hydroxyindoleacetic acid compared to rats only mildly septic with no encephalopathy. The infusion of branched chain amino acids during sepsis had no effect on this deranged brain neurotransmitter profile. Previous results of derangements in the blood-brain barrier transport mechanism combined with the present findings of a deranged brain amino acid and neurotransmitter profile during sepsis may be responsible, at least in part, for the metabolic encephalopathy observed during sepsis and might suggest a common etiology for septic, hepatic, and other metabolic encephalopathies.
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PMID:Brain neurotransmitter profile is deranged during sepsis and septic encephalopathy in the rat. 285 4

A 79-year-old woman with primary biliary cirrhosis was admitted with esophageal variceal hemorrhage. She was initially managed with sclerosing of esophageal varices with no relief from the bleeding. Intravenous Vasopressin was started, but had to be discontinued because of cutaneous changes. A portocaval shunt was performed to control the variceal bleeding. Postoperatively she did poorly from sepsis and hepatic encephalopathy and died 46 days after admission to the hospital.
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PMID:Cutaneous manifestations of intravenous vasopressin therapy. 293 Oct 19

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

We report the clinical features of 7 men (mean age 22 years, range 7-53 years) with congenital hepatic fibrosis (CHF). Five patients presented with variceal bleeding and/or hepatosplenomegaly due to portal hypertension. Cholangitis was the presenting symptom in the other 2 cases. Diagnosis was established by histological examination of a surgical wedge biopsy (4 patients) or needle biopsy (3 patients). A portal-systemic shunting was performed in 6 patients, three times prophylactically. None of the 5 survivors developed chronic hepatic encephalopathy. Recurrent bouts of cholangitis with septicemia and hepatic abscesses were a major complication in 5 patients with a fatal outcome in 2 cases. Six patients had associated small and large cysts in the cortex of both kidneys, compatible with adult-type polycystic disease. One patient developed terminal renal insufficiency. In 3 patients kidney function remained normal at a mean follow-up time of 7.5 years (range 1-18 years). In 2 families (4 cases) an autosomal dominant inheritance of renal disease was suggested. This study demonstrates that CHF is a rare cause of portal hypertension in late childhood and in adults. Cholangitis is a severe and frequently fatal complication. Association with a variety of congenital renal abnormalities is very frequent. However, the association with adult-type polycystic disease as reported in 4 cases is very rare.
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PMID:Congenital hepatic fibrosis. 341 Nov 2

Nine patients with bleeding oesophageal varices, who had not responded to aggressive conservative treatment, underwent emergency transabdominal oesophageal transection and reanastomosis using a mechanical stapling instrument. According to the classification of Child, 2 were graded as Class A, 4 as Class B, and 3 as Class C. Successful control of haemorrhage was achieved in all patients. Three patients died 15-33 days postoperatively. Causes were hepatic failure, sepsis and circulatory insufficiency. Recurrent variceal bleeding occurred in one patient after 15 and 23 months. One patient bled from the oesophageal wall were a clips had slipped after 17 months. One patient required postoperative dilatation due to oesophageal stricture. There was no anastomotic leakage and no cases of hepatic encephalopathy. One patient died after 26 months from an intercurrent disease. The remaining 5 patients are alive and free from symptoms related to varices 6, 20, 24, 25 and 32 months postoperatively. When other measures prove ineffective, transection with the EEA instrument can be recommended to control exsanguinating haemorrhage from oesophageal varices. It seems to be a useful additional procedure to those already in use. For definite assessment and conclusion, however, more experience from additional operations must be gained and longer follow-up is required.
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PMID:Emergency oesophageal transection for uncontrolled variceal bleeding. 348 3

Gamma-aminobutyric acid (GABA) is a potent amino acid neurotransmitter that suppresses normal neuronal activity in the central nervous system. Recently it has been suggested that GABA may play an important role in the pathogenesis of hepatic encephalopathy. In the present study GABA production by 8 common bacterial pathogens was measured during mid-log, stationary and mid-death phases of growth. All bacteria produced some GABA (range: 160-50 250 pmole/ml) with the majority of GABA production occurring during the mid-death phase of growth. These results suggest that the depressed levels of consciousness seen in patients with overwhelming sepsis or advanced liver disease and extraintestinal infection may in part be secondary to increased bacterial GABA production.
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PMID:Gamma-aminobutyric acid (GABA) production by eight common bacterial pathogens. 377 73

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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