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At least 19 recordsLinked to original sources
PubMed1978

Hemorrhagic necrosis of the intestinal mucosa associated with disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC), experimentally induced by endotoxin, caused severe hemorrhagic necrosis of the intestinal mucosa in dogs. Microscopic observation showed tortuous thrombus formation in the microcirculation of the villi. Ligation of the pancreatic and bile ducts, or administration of heparin protected the mucosa from hemorrhagic necrosis, while systemic administration of tranexamic acid increased the intestinal mucosal lesion. Local pretreatment of the intestinal mucosa by Trasylol or tranexamic acid reduced the degree of hemorrhagic necrosis. It is concluded that intravascular coagulation in the microcirculation of the intestinal mucosa, as well as pancreatic proteases, play a role in the pathogenesis of hemorrhagic necrosis in the intestine associated with DIC.

Animals↗
PubMed1977

Pitfalls in peripheral vascular surgery: Disseminated intravascular coagulation.

Disseminated intravascular coagulation is infrequently encountered in the practice of peripheral vascular surgery. Nonetheless, it has devastating and often fatal effects. In our series of eight cases, the mortality rate was 62.5 per cent. A better understanding of the basic disease process as prompted by this review, earlier diagnosis, and rational treatment should lead to higher survival rates and lowered morbidity.

Aged↗
PubMed1976

Rat liver macrophages will not phagocytose fibrin during disseminated intravascular coagulation.

Disseminated intravascular coagulation was induced in rats by injection of a silver colloid suspension or thrombin. Ten min after the injection of colloid, fibrin deposits were observed light microscopically in all major organs. At 30 min, fibrin was no longer present. In rats treated with antifibrinolytics (epsilon-aminocaproic acid or Trasylol) fibrin was still present at 30 and 60 min. Interaction of fibrin with Kupffer cells was studied by electron microscopy. At 3, 10, and 20 min after the colloid injection, all fibrin occurred extracellularly, close to the surface of Kupffer cells. At 30 min, all fibrin had disappeared. In rats pretreated with antifibrinolytics, too, all fibrin was found extracellularly at 10, 30, and 60 min. Comparable results were obtained when thrombin was used to induce coagulation. It is concluded that removal of native fibrin from the circulation by Kupffer-cell phagocytosis is unlikely.

Animals↗
PubMed1976

Disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) is a syndrome of deposition of platelet-fibrin thrombi in the microcirculation, with consumption of platelets and clotting factors and possible clinical features of bleeding or thrombosis or both. It may be produced by activation of coagulation, platelet aggregation or endothelial damage. It is not a primary disease, but a common and important complication of many serious illnesses, especially sepsis, carcinoma and obstetrical accidents. Shock and acidosis are frequent precipitating factors, and vitamin K deficiency is a common complicating factor. DIC usually produces no clinical features, but it may give rise to bleeding, ischemic organ damage or shock. Although its clinical contribution is often difficult to separate from that due to the underlying disease, DIC remains the commonest cause of a generalized bleeding tendency in acutely sick patients. Laboratory confirmation consists of the demonstration of thrombocytopenia, coagulation impairment, hypofibrinogenamia, raised levels of fibrin degradation products, and positive results of para-coagulation tests. The most important therapeutic measure is control of the underlying disease, but replacement therapy and heparin may be required, especially if bleeding is significant and the process is not acute and self-limited.

Disseminated Intravascular Coagulation↗
PubMed1979

Activation of coagulation and disseminated intravascular coagulation in the newborn.

Human newborns have certain hemostatic "deficiencies" which seem to be peculiar to this period of life, such as reduced factors II, VII, IX, X, XI, and XII, reduced antithrombin III levels, and reduced plasminogen levels. However, they are capable of activating the coagulation mechanism to elicit either the entity of disseminated intravascular coagulation or the occurrence of localized and diffuse thrombotic events. The mechanisms involved have yet to be defined. Evidence has been presented to suggest that preterm infants may manifest a variant form of disseminated intravascular coagulation in which thrombocytopenia is not present.

Adult↗
PubMed1978

[Acute ischemic gastric mucosal and duodenal lesions in dogs: "stress ulcer" after experimental disseminated intravascular coagulation].

Experimental disseminated intravascular coagulation (DIC) without considerable effect on blood pressure is shown to produce within 80 min acute mucosal bleeding in stomach and duodenum. A documented high degree of tissue hypoxia caused by mucosal microthrombosis is necessary for the genesis of mucosal lesions. These results stress the necessity to look for DIC in patients with upper gastrointestinal "stress ulcers".

Animals↗
PubMed2026

Coagulation activation is associated with genomic-instability-related features in TP53-mutated AML and MDS: routine laboratory patterns beyond classical disseminated intravascular coagulation.

BACKGROUND: Disseminated intravascular coagulation (DIC) is a serious complication of acute myeloid leukemia (AML) associated with poor prognosis. In TP53-mutated AML and myelodysplastic syndrome (MDS), however, the classical ISTH criteria rarely identify overt DIC, although bleeding and thrombotic complications are well documented in acute leukaemia. We hypothesized that these patients exhibit a lower-grade, subclinical coagulation activation that is associated with the underlying genomic-instability-related features of TP53-mutant disease. METHODS: We retrospectively analyzed 107 consecutive patients with TP53-mutated AML (n = 52) or high-risk MDS (MDS, n = 55), median age 65 years, diagnosed and initially evaluated at our centre between 2018 and 2025. Seven routine coagulation markers and 46 co-mutated genes were evaluated for associations with overall survival (OS) using univariate and multivariable Cox regression, continuous dose-response modeling, and unsupervised k-means clustering. Internal validity was assessed by 1000 bootstrap resamples. RESULTS: Overt DIC according to ISTH criteria was rare (15%). Subclinical activation was common: 50% of patients had a D-dimer &#x2265;1&#xa0;&#x3bc;g/mL, 41% a fibrinogen &#x2265;4&#xa0;g/L, and 29% an INR &#x2265;1.2. In univariate analysis, D-dimer, fibrinogen, INR, prothrombin time, and activated partial thromboplastin time were each associated with OS (HR 1.33-1.38 per SD; all p < 0.05). Complex karyotype correlated with higher D-dimer (median 1.39 vs. 0.60&#xa0;&#x3bc;g/mL, p = 0.022) and fibrinogen (3.91 vs. 2.53&#xa0;g/L, p = 0.007), while TP53 variant allele frequency (VAF) showed modest positive correlations with D-dimer (&#x3c1; = 0.21), INR (&#x3c1; = 0.27), and PT (&#x3c1; = 0.27; all p < 0.05). Clustering identified three coagulation phenotypes: Silent (51%), Thrombo-inflammatory (31%), and Consumption-like (18%), showing a graded but statistically non-significant gradient in molecular features and a stepwise decline in median OS (14, 10 and 8 months; log-rank p = 0.041). After adjustment for complex karyotype, TP53 VAF, and favorable co-mutation count, the Consumption-like phenotype was associated with a non-significant increased risk (HR 1.83, 95% CI 0.92-3.65, p = 0.084), whereas favorable co-mutation pathways remained independently protective (HR 0.56, 95% CI 0.35-0.90, p = 0.016). CONCLUSION: In TP53-mutated AML/MDS, coagulation activation intensity is associated with the degree of genomic instability. The three phenotypes may add biological resolution beyond classical DIC and cytogenetic risk groups, but represent laboratory patterns rather than validated bleeding or thrombosis prediction tools. However, after accounting for genomic features, phenotypes were not independent predictors of outcome, with complex karyotype, TP53 VAF, and favorable co-mutation count driving prognosis. Because treatment intensity and other clinical confounders were not available, these survival associations are hypothesis-generating. Coagulation profiling remains inexpensive, widely accessible, and offers a practical window into disease biology that warrants prospective validation.

TP53↗
PubMed1992

Organ damage in shock, disseminated intravascular coagulation, and stroke.

Disseminated intravascular coagulation (DIC) may cause multiple organ failure. Although DIC may cause capillary occlusion in any and all organs, the lungs, liver, kidneys, gut, heart and brain are particularly affected. Focal brain necrosis can also be caused by DIC. Fibrinolytic therapy will often restore significant blood flow to the capillaries of the lungs. This results in significant increase in lung function because the lung is more resistant to actual necrosis and will resume function once circulation is restored. Administration of fibrinolytic therapy will also prevent liver and kidney failure if started within four hours after trauma. This therapy, when given in low doses intravenously over a twenty-four hour period, has little effect on the coagulation mechanism, and abnormal bleeding, therefore, has not been a concern. It is speculated that if plasminogen activators are effective and safe for treating the intravascular clots of DIC, then perhaps they would be effective in treating other types of intravascular coagulation in the brain, such as various types and degrees of stroke.

Aged↗
PubMed1977

Multiple bone marrow necrosis and disseminated intravascular coagulation.

Pancytopenia and disseminated intravascular coagulation (DIC) developed in a 62-year-old woman. Scattered granulomatous nodules in the bone marrow, composed of numerous eosinophilic concentric spherules with amorphous eosinophilic deposits and reticulin fibrosis between them, resulted in the destruction of the bone marrow architecture. These rare morphologic appearances in the bone marrow may have been caused by lipogranulomatosis and multiple bone marrow infarctions, which were subsequent developments to DIC. Such a process is believed to have induced a lethal secondary hypoplastic anemia.

Anemia, Aplastic↗
PubMed1977

A clinicopathological study on cardiac lesions in 64 cases of disseminated intravascular coagulation.

Diagnosis of disseminated intravascular coagulation (DIC) was made in 64 cases (16.2%) among a total of 395 autopsy cases. There were 31 men and 33 women. Their ages ranged from 31 to 91 years (mean 76.3). Underlying diseases were mainly malignancy and sepsis. Fresh cardiac lesions were found in 40 cases (62.5%). Coronary thrombosis was found in 13 cases (20.3%) and myocardial necrosis in 24 cases (37.5%), with acute myocardial infarction in 9 and focal necrosis in 15. Nonbacterial thrombotic endocarditis was found in 17 cases (26.6%), mural thrombi in 11 (17.2%), and bleeding of the heart in 11 (17.2%). Platelet count, fibrinogen and euglobulin lysis time were not correlated with myocardial necrosis nor coronary thrombosis. Increase of fibrin degradation products correlated with the presence of coronary thrombosis with or without myocardial necrosis. DIC was found with a high incidence in the aged, and many of them were complicated with fresh cardiac lesions. Development of acute myocardial infarction depends on the small thrombi in the severe stenosis of the main coronary arteries or on the multiple microthrombi in the peripheral coronary branches.

Adult↗
PubMedDate not supplied

[The disseminated intravascular coagulation syndrome and infection].

The disseminated intravascular coagulation syndrome (1) Definition. History. (2) Etiopathogeny of the disseminated intravascular coagulation syndrome. (3) The clinical and laboratory diagnosis of the disseminated intravascular coagulation syndrome. (4) The principal infections in which the disseminated intravascular coagulation syndrome has been described: bacterial, viral, rickettsial, parasitic, mycotic. (5) Treatment of the disseminated intravascular coagulation syndrome.

Aminocaproates↗
PubMed1979

[Experimental therapy of disseminated intravascular coagulation by streptokinase administration].

Disseminated intravascular coagulation was induced in dogs by infusion of tissue thrombokinase. Its course was followed by coagulation tests, determination of the rate of microthrombosis, and measurement of organ functions and oxygen consumption. The therapeutic result of streptokinase administration at an early stage of pathological changes is demonstrated by improvement of the disturbed organ functions and oxygen supply as well as by the decrease in plasma-haemoglobin level. When streptokinase was administered at an advanced stage of organ damages, they remained irreversible, although repatency of the microvasculature had been reached.

Animals↗
PubMed1977

Disseminated intravascular coagulation.

The diagnosis of disseminated intravascular coagulation associated with intracranial pathology is discussed. This pathological entity is characterized by a diffuse bleeding diathesis. Laboratory studies suggest a consumption of all clotting and fibrinolytic factors with an elevation of fibrin split products as a sign of the fibrinolytic activity. The treatment consists of the administration of packed platelets and fresh frozen plasma to replace the consumed coagulation factors. Heparinization is recommended early to prevent further consumption of coagulation factors and epsilon-aminocaproic acid is recommended later after acute fibrinolysis is diagnosed. Constant coaguloanalytic monitoring is necessary. Although the etiology with massive injury to brain tissue is possibly secondary to autotransfusion of brain tissue thromboplastin, other causes such as hypotension, anoxia, acidosis and hemolysis must be considered.

Blood Coagulation Tests↗