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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 23 year old primipara with EPH gestosis after caesarean section suffered massive disseminated intravascular coagulation resulting in anuria, respiratory failure, gastrointestinal bleeding and disturbance of liver function. By treatment with antithrombin-III concentrates, fresh blood and fresh frozen plasma we were able to normalise coagulation disorders and to restore organ functions. Causes and therapeutical management of these diseases are discussed.
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PMID:[Successful therapy of consumption coagulopathy in EPH gestosis with multiple organ failure]. 649 88

Anaphylactoid shock, disseminated intravascular coagulation, and anuric renal failure requiring dialysis occurred in a patient receiving zomepirac sodium for toothache. Although renal function showed gradual improvement after seven days of anuria, the recovery was slow and incomplete. Renal biopsy three weeks after the onset of renal failure revealed evidence of focal renal cortical necrosis. Association of zomepirac administration with renal cortical necrosis is not known to have been previously demonstrated. This observation adds another dimension to the previously reported renal complications of nonsteroidal anti-inflammatory agents, especially zomepirac. The proportions of lymphocyte subsets, as defined with monoclonal antibodies, and the proliferative response to mitogens were normal. The patient's lymphocytes showed no proliferative response to zomepirac. Serum complement components and immunoglobulin levels were within normal limits, and radioallergosorbent testing gave negative results. The mechanism of anaphylactoid reaction to zomepirac in this case, therefore, remains unclear.
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PMID:Focal renal cortical necrosis associated with zomepirac. 673 66

A 32-year-old patient without previous medical history died within three weeks of acute Budd-Chiari syndrome with massive thrombosis of the subdiaphragmatic venous system. No definite cause could be elicited. The course of the disease was complicated by anuria attributed to hepotorenal syndrome. Laboratory tests demonstrated major fibrinopenia. Detailed study of the haemostatic system was suggestive of hepatic failure associated with consumption coagulopathy of obscure origin.
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PMID:[Budd-Chiari syndrome with massive thrombosis of the subdiaphragmatic venous system and major fibrinopenia (author's transl)]. 711 Sep 75

The renal venous thrombosis is mostly produced by severe dehydration. The following, however, are also predisposing factors: infections, birth traumata, paranephritic processes, lack of oxygen, diabetes of the mother and cyanotic heart defects. The diagnosis is correctly made by means of the palpable flank tumor, the macrohematuria, together with the urogram and sonography. The most urgent therapeutic measure is the balancing of the water and electrolyte deficit to eliminate the dehydration, i.e. the existing oliguria or anuria. The therapy is primarily always conservative. In the event of a consumption coagulopathy, a therapeutical attempt can be undertaken with heparin but if this is unsuccessful, an immediate nephrectomy must be performed. A further nephrectomy will be necessary if hypertony persistent infection and renal atrophy occur. Two infants with renal venous thrombosis were used for this study on the causes and diagnosis of, and the therapy for the illness.
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PMID:[Renal venous thrombosis in the newborn (author's transl)]. 746 39

The maternal mortality rate associated with eclampsia ranges from 100 to 6000 per 100,000, and the perinatal mortality rate ranges from 150 to 400 per 1000. Both eclampsia and its preceding condition, pregnancy-induced hypertension, occur in varying degrees in different parts of India. The warning signs of imminent eclampsia are 1) systolic blood pressure of 160 mmHg or more on two occasions six hours apart when the patient is on bed rest; 2) proteinuria of 5 g or more in 24 hours or 3 + or more by semiquantitative assay; 3) oliguria or anuria; 4) cerebral or visual disturbances; 5) pulmonary edema or cyanosis; and 6) epigastric/right hypochondriac pain, impaired liver function, and thrombocytopenia and coagulation disorders. Eclampsia is classified as the acute fulminating type, which can occur without warning, and the insidious type. Most cases (61%) show onset of eclampsia during the prenatal period. Treatment of eclampsia involves 1) control of convulsions (through an injection of magnesium sulphate or diazepam or the intravenous administration of phenytoin); 2) correction of hypoxia and acidosis; 3) a gradual lowering of blood pressure with hydralazine hydrochloride, nifedipine, atenolol, labetalol, oxprenolol, or metoprolol); and 4) steps to effect delivery. Diagnosis of HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) requires a complete blood count, blood film for platelet count and red blood cell fragmentation, and a coagulation screen for diagnosis of disseminated intravascular coagulation. Efforts to induce delivery in cases of prenatal eclampsia can take place 12-24 hours after convulsions have stopped. There is no reason to prolong pregnancy in the interests of the fetus, and in some cases Cesarean section may be required. Adequate prenatal care should allow the identification of almost every potential case of eclampsia and allow the prompt treatment of pre-eclampsia or termination of pregnancy when necessary. Medical staff must receive proper training to diagnose pre-eclampsia and treat the condition.
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PMID:Eclampsia. 765 39

We report the case of a premature female newborn of the 35th gestational week with a congenital mesoblastic nephroma. The tumor was prenatally diagnosed in the 32nd week of gestation. By close sonographic controls, rapid enlargement was verified towards the end of the 35th week of gestation. This was probably caused by hemorrhage into the tumor. Anemia and postnatal disseminated intravascular coagulation followed. Cesarean section was done, because the anemia was suspected by Doppler sonographic evaluation. Disseminated intravascular coagulation could not be sufficiently controlled by conservative means but only by surgical removal of the tumor. The tumor turned out to be a congenital mesoblastic nephroma by histologic evaluation. Despite postoperative anuria and catecholamine dependency, our patient eventually showed a very favourable outcome. Diagnosis, clinical behavior and therapy of this tumor with a generally good prognosis are described and discussed.
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PMID:[Disseminated intravascular coagulation caused by prenatal hemorrhage into a congenital mesoblastic nephroma. Case report]. 839 75

The causative organisms, clinical manifestations, factors influencing prognosis, and other epidemiological characteristics of 81 episodes of bacteremia due to gram-negative organisms, in non-neutropenic patients, were studied retrospectively during a 3-year period (1992-1994) at the Department of Internal Medicine of the University Hospital of Heraklion, Crete, Greece. The gram-negative bacteremia incidence was 2% and the overall mortality 12%. All 81 patients had fever; Escherichia coli was the most frequent organism isolated (from 47 patients--58%) and was associated with shock (9/47), disseminated intravascular coagulation (DIC) (8/47), anuria (5/47), adult respiratory distress syndrome (ARDS) (3/47), and pneumonia (1/47). Other less frequent gram-negative microorganisms were Klebsiella spp. (ten patients; 12%), Pseudomonas spp. (7; 7%), Salmonella spp. (5; 6%), Enterobacter spp. (5; 6%), Proteus spp. (3; 3.4%), Stenotrophomonas spp. (3; 3.4%), and Acinetobacter spp. (1; 1.2%). ARDS. shock, DIC, anuria, presence of central venous catheter, urinary catheter, unknown origin of infection and inappropriate treatment were significantly associated with a higher death rate. Early initiation of appropriate therapy was the most important intervention that favorably affected the outcome of gram-negative bacteremias in this patient population.
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PMID:Gram-negative bacteremia in non-neutropenic patients: a 3-year review. 964 6

Six patients with severe and complicated falciparum malaria (6.7 +/- 2.7 WHO criteria) were admitted to our Intensive Care Unit. All patients acquired the disease while travelling in tropical Africa without appropriate chemoprophylaxis. The clinical manifestations included hyperpyrexia (all patients), chills (4), sweating (2), asthenia (3), anorexia (2), headache (1), arthralgias (1), vomiting (4), diarrhoea or abdominal discomfort (3), jaundice (2) and disturbances of consciousness (4). All patients had anemia, thrombocytopenia, hyponatremia, hypoproteinemia, hypoalbuminemia, hypocalcemia and acute renal failure, in one case associated with anuria. A low grade parasitemia was observed in two patients and a high grade parasitemia (20%-58% of erythrocytes) in four. Exchange transfusion was performed only in high parasitemic patients and all of them survived. All patients were treated with quinine, a sulfonamide and pyrimethamine. Additionally, five patients received oxytetracycline, doxycycline or clindamycin. Three patients required hemodyalisis. Five patients had delirium, coma or seizures. All patients had at least one sign of hepatic impairment: liver enlargement, jaundice or increased bilirubin or aminotransferase levels. Two patients had spleen enlargement. Laboratory findings suggested disseminated intravascular coagulation in four patients. Four patients developed pulmonary changes and three of them required mechanical ventilation. A Swan-Ganz catheter was placed in four patients. In three of them (two with pulmonary edema) the pulmonary capillary wedge pressure was initially increased, which suggested a cardiogenic or hypervolemia mechanism, but soon returned to normal level. One patient with low grade parasitemia died because of adult respiratory distress syndrome after 18 days. In our series, the degree of parasitemia was not related to the severity of the disease.
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PMID:[Severe and complicated malaria. Report of six cases]. 977 80

Hantaviruses are RNA viruses that belong to the genus Hantavirus, family Bunyaviridae. The main reservoir of hantaviruses are rodents. Humans become infected by inhaling particles of dust contaminated with faeces of rodents, that are found In Europe and Asia hantaviruses named: Hantaan, Seoul and Dobrava-Belgrade causing haemorrhagic fever with renal syndrome (HFRS) are prevalent. Typical clinical picture of HFRS consists of renal insufficiency (primarily anuria and then polyuria with disturbances of water and electrolytic balance), hypotension, shock and disseminated intravascular coagulation and fibrynolisis (DIC). The mild form of this disease caused by Puumala virus is found in Scandinavia. North and South America are the regions where the prevalence of viruses: Sin Nombre, Black Creek Canal, Bayou, and New York causing hantavirus pulmonary syndrome (HPS) has been noted. In the course of this disease non-cardiogenic pulmonary oedema requires immediate hospitalisation at intensive care ward with artificial ventilation. Mortality in HPS due to hypotension, hypoxia and shock ranges up to 40%.
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PMID:[Diseases caused by hantaviruses]. 991 18

BACKGROUND: Leptospirosis (LS) and Hantavirus (HV) infection have many common clinical manifestations, including acute renal failure. In as much as clinical experience with these diseases is quite limited in urban centers, we identified cases of Leptospira and HV-induced acute renal failure and compared the clinical course and evolution of these diseases. METHODS: Patients hospitalized with acute renal failure, suspected to be caused by infection, were retrospectively studied over a 13-year period (1985-1998). Based on pertinent clinical data and positive serology, a total of 26 patients were included in the study, 17 patients with LS and 9 patients with HV infection. RESULTS: Both diseases presented as flu-like syndromes with high fever. In LS, 2 patients presented with acute meningitis and died soon after admission. Symptoms and signs from other organs began after the fifth day of illness. Jaundice occurred in 71% of LS patients but not in HV. Hemorrhagic phenomena occurred in both diseases but affected predominantly patients with icteric LS. Anuria or oliguria occurred in 76% of patients with LS and 78% with HV infection. Laboratory studies demonstrated minor transaminase elevations in all patients with LS and in 44% with HV. Hypoprothrombinemia or thrombocytopenia was uncommon, although disseminated intravascular coagulation (DIC) developed in 2 patients that had icteric Ls and major bleeding. Nephropathy was associated with haematuria in 71% with LS and all patients with HV. Proteinuria was evident in 35% of patients with LS compared to 78% with HV. Abnormal chest radiographs were seen in 24% with LS and in 33% with HV. In both diseases, aggressive supportive treatment was given, including hemodialysis or peritoneal dialysis in 4/26 patients. Of the 26 patients, 22 survived and four died. The latter all had LS, and the causes of death were meningitis and DIC with multiple organ failure. Follow-up, after 6 months, showed that renal function had returned to normal in the 22 survivors. CONCLUSION: It is important to include LS and HV infection in the differential diagnosis of acute renal failure. Both diseases present with flu-like symptoms and may be complicated by thrombotic microangiopathy with hemorrhagic phenomena and hepatic and pulmonary involvement. Jaundice should alert the physician to icteric LS, a severe disease associated with significant mortality that requires antimicrobial treatment.
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PMID:Acute renal failure caused by leptospirosis and Hantavirus infection in an urban hospital. 1206 23


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