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

The Kasaach-Merritt syndrome involves the very infrequent symptom complex of "giant hemangioma--thrombocytopenia--coagulation disorder". Hemorrhagic diathesis is here based on consumption coagulopathy. This paper reports upon secondary bleeding after extraction of a tooth in a 25-year-old male affected with this syndrome. Continuation or initiation of anticoagulant therapy is recommended for surgical stomatological treatment on an inpatient basis, and measures to be taken in connection with wound treatment are described.
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PMID:[Kasabach-Merritt syndrome as viewed from a surgical and stomatological standpoint (author's transl)]. 16 16

A case report of a patient with primary fibrinolysis resulting in hemorrhage after an oral surgical procedure has been presented. A comparison was made between DIC and primary fibrinolysis in patients with carcinoma of the prostate gland; etiology, clinical findings, diagnosis, and treatment were discussed.
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PMID:Primary fibrinolysis after oral surgery. 16 85

During a large clinicopathologic study of acute nonlymphocytic leukemia (ANLL), ten patients were identified in whom the leukemic blasts demonstrated striking morphologic and cytochemical similarities and who seemed to form a specific subgroup of ANLL. The patients' leukemic blasts were studied in routine blood and bone marrow preparations and by cytochemical and ultrastructural techniques. In routine smears, the blasts showed no clear evidence of differentiation. Cytochemically, the blasts exhibited strongly positive nonspecific esterase activity, which was completely inhibited by incubation with sodium fluoride, and were myeloperoxidase and sudan black B negative. Ultrastructural features of the blasts were similar to those described for monocytic leukemias. Striking clinical features included the occurrence primarily in young patients, the high frequency of lymphadenopathy at presentation, and the high incidence of post-treatment disseminated intravascular coagulation. Complete remissions were frequently initially obtained with duanorubicin in combination with various other agents and later in the disease with VP16-213. Based on the cytochemical and ultrastructural features, we concluded that this form of ANLL was a variety of acute monocytic leukemia. Recognition of the entity is important for optimal therapy.
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PMID:Acute monoblastic leukemia: diagnosis and treatment of ten cases. 16 29

Generalized Shwartzman reaction (GSR) was induced in rabbits by two intravenous injections of endotoxin 24 hours apart. Consumption coagulopathy was found in all cases. Histological investigations showed an abacterial endocarditis (thrombotica or verruccosa simplex), comparable to the one seen in humans after shock, in 69% of the treated animals. Biopsies of mitral valve were investigated by electron microscopy. In the early stage of GSR the valvular alterations were characterized by an oedema of the entire valve, an increase in the number of microvesicles in the endothelial cytoplasm, and a marked enlargement of endothelial cell surface by numerous cytoplasmic projections. At a later stage autophagic vacuoles, often showing a destruction of their membranes, and degenerative changes in cytoplasmic organelles occurred in many cells of the valve. On the other hand there were cells in the endothelium, which presented a distinctly increased number of Golgi complexes and of cisternae of rough endoplasmic reticulum. In other regions ruptures of endothelial plasmalemma, as well as hemorrhages into the valvular stroma were observed. Thus predestined loci for thrombogenesis were formed. In conjunction with these structural changes three factors may be involved in the formation of endocarditis due to shock: 1. hypercoagulability in the course of consumption coagulopathy, leading to precipitation of fibrin and platelets in the circulating blood; 2. turbulences of the blood flow, which are produced by the closure of the heart valves, and favour thrombogenesis on valves: 3. direct changes of the endocardium during endotoxemia. Quantitative changes in the different compartments of intracytoplasmic organelles in many cells of the endothelium during the later stage of GSR are discussed.
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PMID:Experimental investigations into the pathogenesis of endocarditis due to shock. 17 Sep 5

Review of the coagulation laboratory records and medical records at Memorial Sloan-Kettering Cancer Center over a three year period (1971--1974) revealed 89 patients with disseminated intravascular coagulation (DIC). The diagnosis of DIC was made if laboratory studies showed evidence of quantitative and qualitative changes in fibrinogen and significant thrombocytopenia. The patients included 19 with leukemia (17 acute), 3 with multiple myeloma, 15 with lymphoma, 46 with metastatic solid tumors, (10 lung, 9 breast, 8 gastrointestinal, 12 genitourinary, 7 miscellaneous) 4 with vascular tumors, and 3 without tumor. Other conditions which might have precipitated or initiated DIC such as gram-negative sepsis, liver impairment, or mucin secreting tumors were present in the majority of patients. Bleeding occurred in 75% of the patients and was fatal in 36%. Thromboembolism occurred in 22.5%. Thirteen percent were asymptomatic. Serum lactic dehydrogenase was elevated in over 75% of the patients at the time of, or subsequent to the occurrence of DIC. Treatment with heparin was helpful in only three of twenty patients. Eighty percent of the patients died within one to over 30 days of the onset of DIC. Post mortem evidence of DIC was present in 18 of 43 autopsies. Results of this study indicate that DIC is a frequent complication of a wide variety of tumors and that its occurrence causes morbidity and mortality in a significant number of patients. Treatment with heparin is of little help unless remission is induced and the precipitating factor(s) are reversed.
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PMID:Disseminated intravascular coagulation: experience in a major cancer center. 17 94

Disseminated infection caused by Herpes simplex virus (HSV) type I is described in a previously healthy adult. The clinical course was characterized by progressive hepatic failure, fever, hypotension, atypical lymphocytosis, and disseminated intravascular coagulation. No skin lesions were present and the causal agent was not suspended premortem; however, HSV-I was isolated from autopsy liver, and characteristic histopathological lesions of herpes infection were observed in liver and esophagus.
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PMID:Hepatitis in an adult caused by Herpes simplex virus type I. 18 Dec 86

Herpesvirus hominis (HVH) hepatitis, a rarely recognized manifestation of HVH infection in adults, occurred in a 36-year-old woman who had received prednisone therapy for pemphigus vulgaris continuously for seven years. After an acute terminal illness that was characterized by fulminant hepatic failure and disseminated intravascular coagulation (DIC), postmortem examination disclosed massive hepatic necrosis. Herpesvirus hominis (type 1) was isolated from the liver. The association of disseminated HVH infection with impaired immunologic defenses, as well as the occurrence of DIC in association with acute hepatic failure, are discussed. Greater awareness of the clinical manifestations of HVH hepatitis should lead to early diagnosis, although sucessful modes of therapy await development.
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PMID:Herpesvirus hominis hepatitis and disseminated intravascular coagulation. Occurrence in an adult with pemphigus vulgaris. 18 74

Leukocytes from donor blood were separated by ficoll/Urovison density centrifugation into granulocytes, lymphocytes and monocytes. The cell fractions were suspended in a culture medium to which endotoxin of Salmonella enteritidis was added at a final concentration of 10 microgram/ml. Endotoxin-stimulated monocytes developed a very high tissue factor (thromboplastin) activity while in granulocytes an only negligible amount of tissue factor activity was detectable. The tissue factor activity measured in the preparation of the lymphocytes can be explained by contamination with monocytes. Eelectron microscopic studies showed the lysosomes of all monocytes to be enlarged and activated. Only a fraction of the granulocytes appeared degranulated with prominent vacuoles containing inclusion bodies. Possibly the high tissue factor activity of the monocytes triggers the development of the disseminated intravascular coagulation in the Shwartzman phenomenon.
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PMID:The procoagulant activity of human granulocytes, lymphocytes and monocytes stimulated by endotoxin. Coagulation and electron microscopic studies. 19 2

A previously healthy 37-year-old woman had a 5-week febrile disease starting 10 days after delivery, which was complicated by disseminated intravascular coagulation and treated with fresh blood transfusions. She developed severe encephalitis with coma. She also had signs of perimyocarditis and enlargement of liver and lymph nodes. The encephalitis was completely reversible. There was a 16-fold rise in complement-fixing antibodies against cytomegalovirus.
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PMID:Cytomegalovirus infection associated with severe encephalitis. 19 92

Hematological studied were carried out serially in the rats transplanted subcutaneously with Yoshida ascites hepatoma AH-109A. Significant changes were observed in fibrinogen level, fibrinogen degradation products, recalcification time, platelet count, and fragmentation of red blood cells. Formation of thrombi was revealed in the vessels of tumor tissue morphologically from early stage when the tumor grew to a palpable size. Thrombi were formed also in the arterioles of the lungs in the terminal stage. Bleeding tendency was noted in some cases at death. These findings suggested the experimental induction of a type of disseminated intravascular coagulation. The systemic changes of the blood occurring in the terminal stage were preceded by localized intravascular coagulation and fibrinolysis in the tumor in early stage of tumor growth.
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PMID:Hematological alterations in tumor-bearing rats, with reference to pathogenesis of chronic type of disseminated intravascular coagulation syndrome. 20 34


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