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)

During 1983 and 1984 12 patients suffering of acute renal failure aged 65 or more were treated in the Intensive Care Unit. All patients were oliguric at the moment of the acceptance. In six of them laboratory parameters: the renal failure index and the excretional fraction of filtered sodium indicated functional oliguria. In other six patients acute renal failure of the parenchymal type was present with a renal failure index from 3.8 to 34.7. Four patients were treated with the extracorporeal hemodialysis because of the lack of the adequate diuresis following the rational treatment. The patients suffered from: cardiogenic shock, sepsis, dehydration, acute pancreatitis, coma during medicamentous intoxication, osteomyelitis, urosepsis and thrombosis of the abdominal aorta. The urine osmolality was not specific enough for the differentiation of the type of acute renal failure, the urine: plasma osmolality ratio and the creatinine urine: plasma ratio were of greater values and the renal failure index and the excretional fraction of filtered sodium were referring parameters for the differentiation of the type of acute renal failure.
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PMID:The characteristics of acute renal failure in older persons. 371 62

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

In order to determine the effects of steroid administration on the metabolic response to isolated closed-head injury, a longitudinal study was performed. Metabolic indices were prospectively evaluated for the first 5 days postinjury in six patients who received steroids and 10 patients who did not. Patients were carefully screened to eliminate those with associated injuries as well as those with abnormalities due to sepsis. Other than steroid administration, a uniform treatment regimen was used in both groups. Metabolic indices measured on postinjury Days 1, 3, and 5 were analyzed. In addition, data were compared to results in large data banks obtained both from overnight-fasted patients (fasted controls) and from polytrauma victims (stressed controls). Both treatment groups were comparable with respect to age, mean Glasgow Coma Scale scores on admission and on Day 5, and initial intracranial pressure. Metabolic data indicated significantly higher levels of nitrogen excretion and somatic protein mobilization in steroid-treated patients than in patients not receiving steroids. In both groups, glucose levels, the lactate/pyruvate ratio, and branched-chain amino acid levels (all metabolic indices that correlate well with level of stress) initially corresponded to values for stressed controls. By Day 5, values for these variables were similar to fasted controls for the group not receiving steroids. In patients receiving steroids, however, the data remained similar to those for stressed controls. It is concluded that steroids prolong the metabolic abnormalities associated with the initial phase of head injury. In view of inconclusive data regarding benefit from steroid administration, serious questions must be raised regarding the use of these catabolic agents in this setting.
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PMID:Physiological and metabolic response to isolated closed-head injury. Part 2: Effects of steroids on metabolism. Potentiation of protein wasting and abnormalities of substrate utilization. 381 33

In pigs subtotal ischemic liver cell necrosis was induced 4 days after auxiliary transplantation of 60% of the liver of an MLC-compatible donor (ATPL group, n = 13). In control animals (n = 14) temporary liver ischemia was preceded by division of the hepatic ligaments and creation of an end-to-side portacaval shunt. In the ATPL group six animals died of gastric hemorrhage, intestinal strangulation, or sepsis. The remaining seven animals survived in excellent condition until sacrifice 26 days after the induction of liver ischemia. Excellent graft function was demonstrated by uptake and excretion of 99mTc-HIDA at cholescintigraphy, ammonia detoxification, synthesis of clotting factors and glucohomeostasis. EEG recordings in the animals that underwent transplantation did not change from preischemic levels. Evidence of hepatic regeneration was found in the transplanted livers but could not be demonstrated in the damaged host livers. The control animals died in coma within 72 hours. These results indicate that auxiliary transplantation of a partial liver provides metabolic support and improves survival in animals with induced acute liver failure.
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PMID:Auxiliary transplantation of part of the liver improves survival and provides metabolic support in pigs with acute liver failure. 390 50

A scoring system to assess disease severity in children, based on therapeutic and diagnostic interventions, is suggested. The charts of 475 consecutive admissions to a multidisciplinary pediatric intensive care unit (PICU) were reviewed and therapeutic and diagnostic interventions (TDI) associated with more than 20% mortality identified. These were scored: TDI associated with 20-30% mortality - 1 point; 31-40% - 2 points; 41-50% - 3 points and more than 51% - 4 points. According to these values, a Pediatric Therapeutic and Diagnostic Intervention Score (PTDIS) was calculated for each patient. The study population may be divided, according to PTDIS and mortality, into three groups: moderately severe disease associated with up to 2.7% mortality and PTDIS less than 20; severe disease associated with up to 25% mortality and PTDIS less than 35; critically ill patients with more than 50% mortality and PTDIS greater than 36. PTDIS in survivors was 15.2 +/- 0.6 (mean +/- SE) and 43.6 +/- 1.1 in non-survivors. Pearson's correlation between PTDIS and mortality was R = 0.7162 at a significance level of p less than 0.0001. PTDIS and mortality were not found to be significantly correlated with sex, age or duration of hospitalization in the Unit. Sepsis, central nervous system infections and burns were the primary diseases, and shock, coma and patients after cardiopulmonary resuscitation the indications for admission to the Unit, associated with the highest mortality and PTDIS. This study demonstrates the efficacy of the suggested PTDIS system in accurately assessing severity of disease in a PICU patient population.
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PMID:Scoring system to assess disease severity in children. 396 97

During a 12-month prospective study there were 125 visits to the Harlem Hospital Emergency Room for symptomatic hypoglycemia. Sixty-five patients had obtundation, stupor, or coma; 38 had confusion or bizarre behavior; 10 were dizzy or tremulous; 9 had had seizures; and 3 had suffered sudden hemiparesis. Diabetes mellitus, alcoholism, and sepsis, alone or in combination, accounted for 90% of predisposing conditions; others included fasting, terminal cancer, gastroenteritis, insulin abuse, and myxedema. Average blood glucose levels were lower among comatose than among obtunded patients, but overlap was considerable, and overall there was little correlation among cause, blood glucose levels, and symptoms. Although mortality was 11%, only one death was attributable to hypoglycemia per se, and only four survivors had focal neurological residua.
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PMID:Hypoglycemia: causes, neurological manifestations, and outcome. 400 66

A case of heatstroke is reported in a young recruit who participated in a 4-km march at night. Body temperature was not measured at the time of collapse. Hyperventilation and aggressive behavior misled to the incorrect diagnosis of hysteric reaction. Upon arrival at the Medical Center 4h later, the patient experienced deep coma, renal failure, shock, and uncontrolled bleeding. Inspite of intensive treatment, the patient died 27 h after collapse. A positive blood culture suggests the involvement of septicemia in the fulminant picture of the disease. The importance of immediate measurement of rectal temperature in any case of collapse after exercise is emphasized.
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PMID:Fatal heatstroke after a short march at night: a case report. 400 79

8 patients suffering from severe head injury (Glasgow Coma Scale score of 3-5) were treated with the calcium influx blocker nimodipine (2-3 mg/h) for a traumatic cerebral vasospasm. In every case the spasm involved the frontal region of the circle of Willis with the first two segments of the anterior and middle cerebral artery. Control angiograms, recorded in 6 patients, revealed a dilated or normalized lumen of the vessels that the first angiography had revealed to be spastic. The intracranial and the mean arterial pressure were not altered by nimodipine during simultaneous neurosurgical intensive care therapy (dexamethasone, mannitol, relaxation, and controlled respiration for 2-3 days). Monitoring of the somato-sensory evoked potentials (SEP) showed a distinct improvement of the cortical response within 7 days. One patient died of sepsis 8 days after the accident and one remained in a vegetative state. The remaining patients reached Glasgow Coma Scale scores of 13.0 +/- 1.1. within 8.6 +/- 2.2 days, the initial scores having been 4.1 +/- 0.8. One year after their accident all the patients were once again fully able to work. The survival quality was therefore better than that reported in the literature for patients in similar conditions. We conclude from these preliminary results that calcium influx blockers can be used successfully in the therapy of traumatic vasospasm and of severe head injuries. A study involving a larger number of patients is currently in progress.
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PMID:Treatment of cerebral vasospasm following severe head injury with the calcium influx blocker nimodipine. 401 Aug 64

Cisplatin plus 5-FU appears to have significant additive activity in various tumors, such as head and neck carcinoma and esophageal cancer. A partial explanation for this may be drug synergism, which has been noted in the L1210 leukemia model. Based on these data, a prospective trial of weekly bolus 5-FU (15 mg/kg) and cisplatin (60 mg/m2) given every 3 weeks was initiated at Indiana University. Forty-one patients, of whom 38 are fully evaluable for response, were treated with these two drugs. Ten partial and one complete response (complete + partial response rate = 29%) were observed in the 38 evaluable patients. Thirteen additional patients had stable disease for greater than or equal to 3 months. The median durations of remission and survival time were 6 and 10.3 months, respectively. Myelosuppression was unusually severe, with granulocyte counts less than 1000/mm3 in 65% of patients, including four patients with granulocyte count nadirs less than 100/mm3. Three patients developed granulocytopenic fever, with two drug-related deaths (sepsis, hyperosmolar coma). Nearly all patients had nausea and vomiting, but this was not a treatment-limiting toxic effect in any patient. Although this combination suggests a higher response rate than usually seen with bolus iv 5-FU in colon cancer, a trial comparing 5-FU alone or with cisplatin to determine whether true synergy exists is currently underway.
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PMID:Cisplatin plus 5-FU for the treatment of adenocarcinoma of the colon. 407 11

Twelve fatal cases of encephalopathy associated with sepsis were examined in a ten-year retrospective study. The sources of infection and organisms isolated were variable. Six of the patients had focal neurologic signs; five had seizures. The level of consciousness varied from drowsiness to deep coma, and electroencephalograms revealed diffuse or multifocal abnormalities. Computed tomographic head scans and cerebrospinal fluid examinations were usually unremarkable. Eight patients had disseminated microabscesses in the brain at autopsy. Four patients had proliferation of astrocytes and microglia in the cerebral cortex, a feature associated with metabolic encephalopathies. Additional findings included cerebral infarcts, brain purpura, multiple small white matter hemorrhages, and central pontine myelinolysis. Although sepsis may cause encephalopathy by producing disturbances in cerebral synaptic transmission and cerebral energy production through a toxic mechanism, bacterial invasion of the brain with the formation of disseminated microabscesses is also an important cause.
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PMID:The encephalopathy of sepsis. 408 65


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