Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A Denver peritoneovenous (PV) shunt was inserted in 54 consecutive patients for relief of malignant (24 patients) or cirrhotic (30) refractory ascites. The median age of both groups was 58 years, and the most frequent diagnoses were gastrointestinal (15) or ovarian (7) cancers and alcoholic cirrhosis (25). Median survival time was 1.7 and 3.5 months (range, 0.1-15.5 and 0.1-50.5), and the 1-month mortality 42% and 27%, respectively. Postoperative 24-h urinary output increased by 2-31, and the 1-week weight reduction was 8 and 11 kg, respectively, compared with before shunting. Complete shunt failure was encountered early in two patients, due to catheter malposition and clotting. Four more patients experienced transient failure, for an early dysfunction rate of 11%. A shunt-related operative mortality of 6% was caused by pulmonary oedema (two patients) and sepsis (one patient). Shunt malfunction intervened in almost half (6 of 14) of the cancer patients surviving 1 month but was relieved in all but 1. In 3 of 22 cirrhotic 1-month survivors, the Denver shunt had to be removed owing to clotting or sepsis (2 patients) or revised because of blockage. Seven patients with cirrhosis are alive a median of 18 months (range, 2-51) after PV shunt surgery. Side effects were detected in 22 patients (41%): thromboembolism (9 patients), sepsis (7), initially bleeding oesophageal varices (3), DIC syndrome (2), postoperative hepatic coma (2), ascitic leakage (2), and pulmonary oedema (2). Patients with gastrointestinal cancers or severe cardiac disease did not benefit from the procedure. A history of hepatic encephalopathy or a serum bilirubin level above about 100 mumol/l was a bad prognostic sign. We could confirm the reported considerable morbidity and mortality after PV shunting, but also its efficiency in certain cases. Careful patient selection and follow-up study, timing of operation, and adherence to technical details are mandatory to improve the results.
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PMID:Denver peritoneovenous shunting for malignant or cirrhotic ascites. A prospective consecutive series. 380 91

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

The first reported case, in an adult, of cholestyramine induced hyperchloremic metabolic acidosis is a 70 year old female with a two year history of primary biliary cirrhosis confirmed by histologic and immunologic criteria. After taking cholestyramine II sachets twice daily for two months she presented with lethargy, confusion and drowsiness. Examination revealed confusion, jaundice, signs of chronic liver disease, portal hypertension and hepatic encephalopathy. Laboratory investigations confirmed a metabolic acidosis (pH 7.15) and hyperchloremia. Multiple cultures failed to reveal sepsis and a urinary pH of 4.85 together with tests of renal acidification, excluded renal tubular acidosis. She received 600 mEq of sodium bicarbonate intravenously over 36 hours by which time her mentation, electrolytes and pH were normal. It is presumed that her hyperchloremic metabolic acidosis was secondary to cholestyramine because of the similarity to pediatric reports; the rapid and lasting response to intravenous sodium bicarbonate; the absence of another etiology; normal serum potassium, chloride and bicarbonate despite continued spironolactone therapy after recovery.
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PMID:Cholestyramine induced hyperchloremic metabolic acidosis. 659 13

Management of protein-calorie malnutrition found in 32 patients with severe liver diseases such as fulminant hepatitis and cirrhosis of the liver was carried out using 2 types of synthetic amino acid solution (Hep-OU and Fischer solution) for intravenous and enteral alimentations with rapid monitoring of serum aminogram. Intravenous hyperalimentation of these cases resulted in maintenance of nutritional status with improvement of nitrogen balance and normalization of impaired serum aminogram. During this study, however, nutritional support was initiated only when intractable ascites, upper gastrointestinal bleeding and hepatic encephalopathy were observed. In 2 cases of fulminant hepatitis with sepsis and 3 hepatoma patients with ascites, elemental diet containing maltose and amino acids was used to supply sufficient amounts of nutrients in a minimum volume of water. These techniques with simultaneous monitoring of urinary excretion of 3-methylhistidine and creatinine height index as nutritional parameters make nutritional management easy for patients with liver disease.
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PMID:Nutritional management of patients with severe liver disease by using intravenous hyperalimentation and elemental diet. 676 41

Critical evaluation of 22 cases with serious diffuse purulent or fecal peritonitis treated by open abdomen following surgical intervention. Seven (32%) patients died, three because of continuing sepsis and one because of acute haemorrhagic necrotizing pancreatitis. The three other died of general complications (1 coma hepaticum, 2 massive embolisms; at autopsy their abdominal cavity was entirely cleaned. The therapeutic principle of "open abdomen" in cases of severe purulent and fecal peritonitis will be recommendable.
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PMID:[The "left-open abdomen". Technic, indication and results]. 687 39

Cholecystectomy and common bile duct exploration in cirrhotic patients is associated with an 83 percent mortality if prothrombin time is prolonged 2.5 seconds over control. The causes of death are related to complications of liver disease such as hepatic encephalopathy, ascites, sepsis and hemorrhage. If the prothrombin time is prolonged, major intraoperative blood loss can be anticipated, and blood and plasma transfusion requirements may be massive. Jaundice in the presence of cirrhosis requires careful preoperative evaluation and is most frequently due to hepatocellular disease rather than extrahepatic biliary obstruction. Cholecystectomy and common duct exploration in cirrhotic patients should be performed only for life-threatening complications of biliary tract disease such as empyema, perforation and ascending cholangitis.
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PMID:Cholecystectomy in cirrhotic patients: a formidable operation. 705 56

This report describes light and transmission electron microscopy (LM and EM, respectively) studies of kidneys from five cases of hepatorenal syndrome. The kidneys were removed and fixed for LM and EM between 30 and 120 min after death. All patients had progressive renal failure after admission to the hospital. All cases were jaundiced, had ascites, and exhibited features of hepatic encephalopathy. LM study revealed severe acute tubular lesions (ATL) or, more conventionally, acute tubular necrosis (ATN). EM study demonstrated necrosis of the proximal tubules characterized by swelling, disorganization of the cristae and appearance of dark bodies in the mitochondria, coalescence, fragmentation or displacement of the microvilli, loss of plasma membranes, rupture of the basement membranes, and separation of the cells from the basement membranes. Rupture of tubular basement membranes (tubulorrhexis) and mitochondrial dark bodies suggest an ATN due to ischemia or induced by vasoconstrictor substance(s). Glomerular lesions were infrequent (one in five) and therefore, do not seem to have contributed to renal failure. All cases terminally had extremely low urinary sodium (11 mEq/liter), high urinary potassium (50 mEq/liter), a remarkably low urinary sodium/potassium ratio (0.26, normal = 4.27), and a low urinary osmolality (less than 400 mOsm/kg). From this study we conclude that an ATN of variable severity may be associated with the hepatorenal syndrome. Since this ATN developed without preceding shock, sepsis, or hypotension it is possible that this ATN like that in ischemic acute renal failure may be due to reduced renal blood flow and intense cortical vasoconstriction which has been reported in hepatorenal syndrome. Finally, our data imply that low urinary sodium is consistent with this pathologic lesion in this clinical setting.
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PMID:Acute tubular necrosis in hepatorenal syndrome: an electron microscopy study. 714 28

Peritoneovenous shunts (LeVeen) were placed in 52 patients with intractable ascites due to alcoholic cirrhosis between March 1975 and June 1978. The ascites was defined as intractable if it persisted despite at least six weeks of in-hospital medical management. Only 4.5% of such patients seen during this interval met this criterion by failing to respond to intensive drug and diet therapy. Eight (15%) died five to 60 days postoperatively; six of these did not undergo diuresis. Hepatic encephalopathy and sepsis were important contributing factors. There were 21 late deaths (mean survival, 16 months), primarily related to complications characteristic of this group of cirrhotics: upper gastrointestinal hemorrhage and infection. Twenty-three patients were alive by June 25, 1980, with mean survival of 46 months. Four patients operated on five or more years ago survive without ascites. An accurately placed LeVeen shunt dramatically relieves intractable ascites with improvement in renal function, nutrition, and general health. The operation enables at least partial rehabilitation so that ambulatory care becomes feasible for many of these chronically and seriously disabled patients.
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PMID:Intractable ascites treated with peritoneovenous shunts (LeVeen). A 24- to 64-month follow-up of results in 52 alcoholic cirrhotics. 723 44

Thirty-five children with G6PD deficiency, who presented with acute intravascular haemolysis, were evaluated to define its aetiology, clinical features and ultimate outcome. All were boys with ages ranging from 6 months to 12 years. Pallor of abrupt onset and passage of cola-coloured urine were universal presenting symptoms. Incriminating factors responsible for haemolysis include hepatitis (7), malaria (4), bacterial sepsis (3) and drug intake (24), with more than one predisposing condition existing in some children. Marked elevations in serum bilirubin, coinciding with intravascular haemolysis, was a feature in all the seven children with hepatitis. Azotaemia was noted in 20 patients, of whom 14 did not have oliguria. All four children with malaria presented with protracted renal failure. Therapy focused on maintaining a high urine output in those without oliguria. A total of 15 peritoneal dialyses and five haemodialyses were required in six patients with acute renal failure, all of whom were oliguric. Supportive therapy consisted of blood transfusions and treatment of the predisposing diseases. Thirty-two children recovered completely while three died, the cause of death being severe anaemia and congestive cardiac failure, malaria with oliguric renal failure and hepatic encephalopathy, respectively.
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PMID:Acute intravascular haemolysis in glucose-6-phosphate dehydrogenase deficiency. 750 89

We reviewed retrospectively the clinical records, autopsy protocols and central nervous system tissue sections of 50 patients who underwent orthotopic liver transplantation for end-stage liver disease between 12/83 and 8/93. The postoperative survival period ranged from hours (6), weeks (17), months (17), to years (10). All patients received immunosuppressive drugs from the immediate postoperative period to the time of their death (cyclosporine, steroids; occasionally azathioprine, OKT3, FK506). Nineteen patients had neurological manifestations (hepatic encephalopathy) prior to surgery. Post-transplant neurologic signs and symptoms included: hepatic encephalopathy/altered mental status (11), focal or generalized seizures (9) and stroke (2). In the majority of cases (37) the cause of death was septicemia and/or bleeding diathesis. The neuropathologic findings present in 36 patients could be classified into 3 distinct categories: metabolic disorders: hepatic/anoxic encephalopathy, central pontine myelinolysis (15); cerebrovascular disease: subarachnoid and/or intracerebral hemorrhage, bland or hemorrhagic infarction (23); and infection: bacterial meningitis/cerebritis, multifocal fungal microabscesses, presumptive viral meningitis/encephalomyelitis (10). In conclusion, 72% of 50 patients who came to autopsy after liver transplantation were found to have neuropathologic abnormalities; these abnormalities were predominantly infections and vascular diseases.
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PMID:Neuropathology of liver transplantation. 760 96


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