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

Cerebral fat embolism was established as the cause of death in a 34-year-old man with acute pancreatitis. Encephalopathy complicating pancreatitis may be due to hypoxia secondary to pulmonary fat embolism, cerebral fat embolism, or the complicating syndromes of disseminated intravascular coagulation or hyperosmolality.
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PMID:Pancreatic encephalopathy. 32 Jun 76

The case of a nineteen-year-old women with the cerebral form of malaria tropica is reported. She showed hyperpyrexia, abdominal manifestations, haemolysis and disseminated intravascular coagulation. Cerebral symptoms amounting to grade IV encephalopathy occurred. The patient responded rapidly to the administration of chloroquine, anticonvulsants, dextran, corticosteroids, antipyretics, blood and antithrombin III and her symptoms had almost completely vanished one week after the onset of therapy.
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PMID:[Course and intensive treatment of acute falciparum malaria (author's transl)]. 37 59

Clinical and anatomical studies of a case of malarial encephalopathy are described in a 51 year old man. In view of the typical symptomatology it was important to ascertain an period even brief of stay in an endemic area. Only when this was confirmed the appropriate investigations could be planned (in thic case thick blood drop test) to identify the parassite. The physiopathological mechanisms through which the malarial infection causes the parenchymal lesions are considered. Such lesions according to many Authors are of ischemic nature, due to machanical obstruction of capillaries by the invaded erytrocytes with damage to the endotelial wall and thrombus formation. These lesions cause anoxic and necrotic damage of the parenchyma and, in certain cases, the appearance of serious haemorrhagic syndromes where the initial stage is the conglutination of the erytrocytes followed by disseminated intravascular coagulation syndrome. The importance of this syndrome is emphasized as well AA. the role of the association of the specific antimalarial treatment with the use of drugs against blood conglutination, thrombosis and oedema.
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PMID:[Malarial encephalopathy and disseminated intravascular coagulation (author's transl)]. 77 99

After a short survey on the history of the therapy of liver cirrhosis the importance of the prevention of alcoholism is emphasized. A "liver diet" is regarded as unnecessary, prednisolone is recommended for the treatment of the active cirrhosis. After a short description of the principles of the therapy of biliary cirrhoses, of haemochromatosis and of Wilson's hepatocerebral degeneration the use of restriction of salt, saluretics and aldosterone antagonists in the treatment of ascites is discussed in detail. After description of the conservative therapy of the haemorrhage from varices with the compression sound, intraarterial octapressin infusion and combat against consumption coagulopathy finally the prophylaxis of the hepatoportal encephalopathy with reduction of the protein intake and the restriction of the formation of toxic products of protein metabolism in the intestine by application of neomycin or lactulose, respectively, is described.
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PMID:[Conservative therapy of liver cirrhosis]. 85 44

Endotoxins of gram-negative bacteria and of intestinal origin, insufficiently cleared by the hepatic reticulo-endothelial system are of an increasing interest within the pathogenesis of liver diseases. With purpose to obtain data concerning incidence and course of endotoxaemia in patients with liver cirrhosis an unselected group of these patients, sequentially admitted, was investigated by means of the Limulus-gelation test, regarded as most sensitive to endotoxins. At the admittance, 65% of the patients had endotoxaemia, further 14% developed endotoxaemia later. In total 79% of the patients investigated had endotoxaemia.---Bleeding from oesophageal varices was associated with endotoxaemia in 78%, functional renal impairment in 75%, consumption coagulopathy in 81%, encephalopathy in 77% and a pyrogen reaction in 82% of the patients. Regarding the Limulus assay, the dilution technique was more sensitive in detection of free endotoxaemia as opposed to the chloroform extract. It is concluded from the results that endotoxaemia in patients with liver cirrhosis is frequent and has to be viewed as relevant within the pathogeneses of chronic liver diseases.
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PMID:[Endotoxinemia in liver cirrhosis]. 96 Sep 7

Disseminated intravascular coagulation developed secondary to hepatic necrosis in a 5-year-old Saint Bernard. Although the coagulopathy responded to treatment with heparin, the dog died from the combined effects of gastric hemorrhage and encephalopathy, both of which are complications of hepatic necrosis.
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PMID:Coagulopathy and encephalopathy in a dog with acute hepatic necrosis. 97 48

About 15% of patients with cancer have cerebrovascular lesions, resulting from 4 kinds of disorders sometimes intermingled in advanced disseminated cancer: coagulation disorders, direct effects of the tumor, infections and therapeutic measures. Infarction, hardly less frequent than hemorrhage, mostly complicates lymphoma and carcinoma. Hypercoagulation states, such as chronic disseminated intravascular coagulation, nonbacterial thrombotic endocarditis, and nonmetastatic cerebral venous thrombosis account for about 50% of cases. Tumor emboli, as seen in intravascular malignant lymphomatosis, arteritis related to aspergillus, granulomatous angiitis with or without herpes zoster and radiation-induced atherosclerosis are rarer. Cerebral hemorrhages, excluding bleeding from the metastases of choriocarcinoma and melanoma are mainly associated with leukemia by acute disseminated intravascular coagulation as in promyelocytic leukemia, by leukostasis or by pancytopenia. Both infarction and hemorrhage rarely reveal the neoplasia. Lesions are often small and disseminated, and therefore produce a picture of diffuse acute or subacute encephalopathy rather than acute focal deficits. Finally, there may be no relationship between the cerebrovascular event and the neoplasia, and atherosclerosis or traumatic subdural hematoma may well be the causal factor.
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PMID:[Cerebrovascular complications of cancers]. 130 55

Vitamin E pretreatment significantly prevented E. coli-induced Disseminated Intravascular Coagulation (DIC) in rats (1). DIC, a reduction in fibrinogen and a falling platelet count and diffuse haemorrhage are part of the clinical features of Haemorrhagic Shock Encephalopathy Syndrome (HSES), recognised as a disease entity in the 1980s (2). At the SIDS Conference 1974 Reisinger described the effect of Escherichia coli (E. coli) endotoxin on the rabbit (3). An early effect was a reduction in fibrinogen and a falling platelet count, resulting in the release of relatively large amounts of the neuro-transmitter serotonin, stored in platelets (3, 4). Fibrinogen inhibited the release of serotonin from platelets (24). Serotonin is released from platelets during platelet aggregation (14). Platelet aggregation is inhibited by vitamin E (1). Serotonin is a neuro-transmitter associated with deep sleep, respiratory movements and cardiovascular collapse (3). Death at a later stage involved vascular permeability, edema and haemorrhage. After fibrin-platelet clots had formed DIC was present in lungs, kidneys and other organs (3). Medical researchers in Australia linked almost half of SIDS victims with a poisonous strain of intestinal E. coli bacteria (5). Dietary selenium in the intestinal villous tip is considered a daily modulator of cytochrome P450-dependent metabolism of drugs and toxins absorbed by intestinal mucosa (6). Villous atrophy occurs in HSES (2).
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PMID:Sudden infant death syndrome (SIDS) and the immune response. 146 Nov 72

We describe three infants (aged 9 weeks to 4 months) with the classic features of hemorrhagic shock and encephalopathy syndrome, including sudden onset of shock, neurologic disturbance, bleeding, disseminated intravascular coagulation, and impaired hepatic and renal function. Unlike the cases previously described, all three children recovered rapidly without evidence of long-term neurologic damage. These findings may modify the perception that this disorder has a uniformly bad outcome.
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PMID:Complete recovery from hemorrhagic shock and encephalopathy. 140 12

Hydrocarbon ingestion may result in serious complications such as adult respiratory distress syndrome, encephalopathy, and seizures. Hematologic disorders have appeared to be rare complications of hydrocarbon toxicity. After encountering a case complicated by severe intravascular hemolysis, we reviewed the hospital records of all patients admitted to our pediatric intensive care unit (PICU) because of complicated hydrocarbon poisoning. Three of the 12 PICU patients identified developed intravascular hemolysis, and one developed disseminated intravascular coagulation. One patient required transfusion, but all recovered without sequelae. Intravascular hemolysis may be a more frequent complication of hydrocarbon poisoning than previously recognized.
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PMID:Intravascular hemolysis associated with hydrocarbon poisoning. 160 87


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