Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Shock continues to be associated with a high mortality rate primarily because of delays in diagnosis and therapy. To diagnose shock early, and thereby increase the chances of reversal before there is extensive deterioration of vital organs, one should look for any decrease in pulse pressure, urine output, urine sodium concentration, alertness or any increase in urine osmolarity, tachypnea or tachycardia. Systolic hypotension, oliguria, metabolic acidosis and a cold clammy skin are late signs of shock. The pathophysiology of early hypovolemic shock includes hyperventilation, vasoconstriction, cardiac stimulation, fluid shifts into the vascular system and platelet aggregation. Late shock is characterized by lysosomal breakdown, subsequent release of kinins (especially bradykinin), impaired cell metabolism and organ function, fluid shifts out of the vascular system because of capillary endothelial damage and intravascular coagulation. The primary cause of shock should not be neglected in favor of treating signs, symptoms, and laboratory data. The resuscitation from the shock process itself involves correction of pathophysiologic changes, based on objective trends and responses rather than isolated measurements. A suggested outline of therapies in order of their use includes: 1) correction of the primary problem; 2) ventilation and oxygen; 3) fluid-loading: 4) inotropic agents; 5) correction of acid-based and electrolyte abnormalities; 6) steroids ("physiologic" or "pharmacologic" doses); 7) vasopressors (especially in elderly, severely hypotensive patients); 8) vasodilators (if excess vasoconstriction); 9) diuretics (if oliguric in spite of the above), and 10) heparin (if DIC). The most common errors are 1) late diagnosis; 2) inadequate control of the primary problems; 3) inadequate fluid loading; 4) delayed ventilator assistance, and 5) excessive reliance on and use if vasopressors and diuretics.
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PMID:Shock in the emergency department. 79 60

Twenty-five assessable patients with metastatic melanoma have been entered in a multicenter phase II study of two induction cycles of human recombinant interleukin-2(IL2), 18 x 10(6) IU/m2/d continuous intravenous (IV) infusion on days 1 to 5 and days 12 to 17. Dacarbazine (DTIC), 850 mg/m2 IV bolus was given on day 26. The cycle was repeated at 5 weeks. Maintenance therapy was scheduled 3 weeks after the completion of induction treatment, consisting of IL2, 18 x 10(6) IU/m2/d for 5 days alternating with DTIC, 850 mg/m2 IV every 3 weeks, for a total of 18 weeks. Six patients responded (24%); two complete and four partial. Stable disease was seen in five patients. None of the six patients with more than two sites of metastases responded. Maximum response was observed in the first 3 months of treatment. Progression-free periods of 6 months and longer were seen in the two complete responders (8 and 17+ months), in two of the four partial responders (7 and 12+ months), and in three of the five patients with stable disease (9+, 15, and 17+ months). Toxicity included fever, skin rash, fatigue, anorexia, and diarrhea in most patients. Two patients had a weight gain of more than 10%. Eight patients needed intensive care for the observation and treatment of a myocardial injury (one patient), ventricular tachycardia (one), hypotension and oliguria (four), and sepsis (two). Sequential treatment with IL2 and DTIC appears to be effective but not clearly better than could be expected of IL2 alone.
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PMID:Sequential administration of recombinant human interleukin-2 and dacarbazine in metastatic melanoma: a multicenter phase II study. 187 25

We have recently experienced a case of Vibrio vulnificus septicemia which occurred in a patient with hepatic cirrhosis, and as we were able to give early antibiotic treatment, the patient survived. We would like to report this case here together with another case experienced 2 years ago. Case 1 was a 58-year-old male who was attending our hospital as an outpatient for hepatic cirrhosis. At 5:30 pm on August 8, 1987, he consumed abalone and giant clam and at 9 pm complained of high fever with shaking chills. He was admitted to our department as an emergency case. Cefoperazone was administered resulting in a decline of fever on the following day. During the course of treatment he fell transiently into pre-DIC, but due mainly to the administration of antibiotics his condition was subsided. Case 2 was a 53-year-old male who was under medical care in our hospital for grave hepatic cirrhosis. On October 11, 1985, he consumed sushi and two days later suffered chills and pyrexia. A blood culture revealed Vibrio vulnificus. His condition improved transiently with administration of Cefazolin, but oliguria, hypotension and ascites occurred subsequently, and finally the patient died on the 22nd day.
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PMID:[Two case reports of septic shock due to Vibrio vulnificus with liver cirrhosis]. 250 32

Burn injury causes dynamic alterations in the coagulation and fibrinolysis, and so-called DIC often occurs in burned patients. In this study the clinical significance of heparin therapy combined with antithrombin III concentrate in animal experiments and clinical experiences were discussed. The changes in blood coagulation, fibrinolysis and kidney function and the effect of anticoagulation therapy using heparin were investigated in rabbits with third degree burn covering 35% of the total body surface area. The animals were subjected to determinations for various kidney function tests, blood coagulation and fibrinolysis tests, blood viscosity and hematocrit value before induction of the burn and after 8 and 24 hours respectively. Thirty rabbits were divided into a non-therapy group, an intravenous infusion group, a heparin group, an antithrombin III group, and an antithrombin III plus heparin group and the results were compared among them. Oliguria and a disturbance of kidney function were noted even at hour 8 after burn in the non-therapy group. In the intravenous infusion group urine volume was maintained well although the early stage of non-oliguric renal insufficiency was noted. The changes noted in the intravenous infusion group were prevented almost completely in the heparin group at hour 8, but FENa and CH2O were elevated at hour 24 probably because antithrombin III activity was depressed markedly. In the antithrombin III group and the antithrombin III plus heparin group, however, creatinine clearance was moderately elevated while FENa and CH2O remained unchanged as compared with the values before the burn. The antithrombin III plus heparin group showed slightly better results than the antithrombin III group in Ucr/Pcr ratio, creatinine clearance and CH2O. The results of the present study indicate that it is extremely effective to initiate appropriate fluid infusion therapy immediately after a burn and administer antithrombin III concentrate in combination with or without heparin for the prevention of acute renal insufficiency in patient with a severe burn. The effects of antithrombin III concentrate when used clinically were also discussed.
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PMID:[Alteration in coagulation and fibrinolysis after burn injury and significance of anticoagulation therapy using heparin and antithrombin III concentrate]. 381 36

In pregnancy and puerperium disseminated intravascular coagulopathy may accompany abruptio placenta, intrauterine fetal demise with retained dead fetus, amniotic fluid embolism, endotoxin sepsis, preecalampsia with HELLP and massive transfusion. Clinical signs and symptoms of DIC can include oozing from venipuncture sites and/or mucous membranes, red cell lysis from activation of the complement system, hemorrhage from coagulopathy and possible uterine atony, hypotension from hemorrhage and/or bradykinin release, and oliguria from end-organ insult and hypovolemia/hypotension. Treatment of DIC consists of replacement of volume, blood products, and coagulation components and cardiovascular and respiratory support with elimination of underlying triggering mechanism.
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PMID:Disseminated intravascular coagulopathy in pregnancy: thorough comprehension of etiology and management reduces obstetricians' stress. 1076 41