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PubMed2005

Pathophysiology, diagnosis and treatment of disseminated intravascular coagulation: an update.

Disseminated intravascular coagulation (DIC) is a disorder characterized by an acute generalized, widespread activation of coagulation, which results in thrombotic complications, due to the intravascular formation of fibrin, as well as diffuse hemorrhages, due to the consumption of platelets and coagulation factors. In this review, we briefly report the present knowledge about the pathophysiology and diagnosis of DIC. We also focus on the current standard treatment of overt DIC in clinical practice. Particular attention is given to novel therapeutic strategies, which reflect the important progresses made in the understanding of the pathogenesis of this disorder in the last few years.

Anticoagulants↗
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↗
PubMedDate not supplied

Disseminated intravascular coagulation associated with disseminated cryptococcosis in a patient with acquired immunodeficiency syndrome.

Disseminated intravascular coagulation (DIC) is uncommon in acquired immunodeficiency syndrome (AIDS), despite the high incidence of infectious diseases. We describe an HIV-infected patient presenting with disseminated cryptococcosis, who had clear-cut laboratory evidence of progressively worsening DIC (thrombocytopenia, prolonged prothrombin time and partial thromboplastin time, hypofibrinogenemia, increased fibrin(ogen) degradation products and D-Dimer, reduced antithrombin III), although the clinical signs of the disease were rather scarce. The patient died despite intense treatment, which included heparin and fresh frozen plasma, and DIC was confirmed histologically. It is suggested that, in a patient with AIDS presenting with an opportunistic infection, laboratory signs of DIC should be carefully checked to early recognize this complication and promptly initiate the required therapy.

Acquired Immunodeficiency Syndrome↗
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↗
PubMed2001

Disseminated intravascular coagulation in sepsis.

Disseminated intravascular coagulation (DIC) has been considered a rather rare syndrome characterized by severe bleeding. In fact, both of these beliefs are wrong. Bleeding is fairly rare in DIC. The clotting parameters are usually normal unless the DIC is fulminating. It is usually thought that fibrinogen may be low or absent in DIC. However, afibrinogenemia is rare. Fibrinogen is usually high in DIC because of the high rate of fibrinogen manufacture by the liver in response to stress. DIC is very common and most cases are never diagnosed. This is because it has been hard to find fibrin thrombi in autopsy cases and because acute severe bleeding is uncommon. The reason fibrin thrombi are rare may be because they have been lysed by endogenous fibrinolytic enzymes before the autopsy. The appearance of endogenous fibrinolytic response could be a defense mechanism to lyse the microclots of DIC. In fact, this response is often successful. This defense can be aided by the administration of plasminogen activators that will lyse the clots. Heparin has been used for the treatment of DIC but has proved useless and is, in fact, dangerous. This is because heparin will not dissolve clots and may actually promote platelet agglutination. Administration of plasminogen activators will actually prevent bleeding diathesis.

Animals↗
PubMed1991

[Levels of tissue-type plasminogen activator and plasminogen activator inhibitor 1 in disseminated intravascular coagulation syndrome].

Since disseminated intravascular coagulation (DIC) may directly reflect the abnormal regulation of the fibrinolytic system by endothelial cells, we have measured the levels of tissue-type plasminogen activator (t-PA), type 1 PA inhibitor (PAI-1) and t-PA . PAI-1 complex which is formed as a result of interaction on the two factors, in the plasma of patients with DIC (n = 51) and healthy controls (n = 42). Antigens of t-PA, PAI-1 and t-PA . PAI-1 complex were significantly increased in the DIC plasma (36.4 +/- 25.1, 106.8 +/- 54.7 and 46.6 +/- 34.5 ng/ml, respectively) compared with those in normal plasma (8.5 +/- 4.3, 54.4 +/- 21.2 and 8.6 +/- 3.5 ng/ml, respectively). The molar ratio of t-PA to PAI-1 was much higher in the DIC plasma (1:3) than in normal plasma (1:6), which caused enhancement of the whole fibrinolytic activity in the DIC plasma. These changes resulted in significant consumption of plasminogen, alpha 2-plasmin inhibitor (alpha 2-PI) and a significant increase of plasmin . alpha 2-PI complex (PPI) and D-dimer. These results suggest that t-PA and its specific inhibitor PAI-1 both of which are secreted from endothelial cells into blood, play an important role on the progress of DIC.

Adult↗
PubMed2000

Successful initial treatment with weekly etoposide, epirubicin, cisplatin, 5-fluorouracil and leucovorin chemotherapy in advanced gastric cancer patients with disseminated intravascular coagulation.

BACKGROUND: Acute disseminated intravascular coagulation (DIC) is a rare but severe complication of gastric adenocarcinoma. Conventional treatments, such as fresh frozen plasma, platelet replacement and heparin injections, are disappointing. The only way to correct this fatal condition is to control the underlying cancer promptly by effective chemotherapy. Here the successful initial control of acute DIC in gastric cancer patients with weekly EEPFL chemotherapy is reported. METHODS: Advanced gastric cancer patients complicated with acute DIC were eligible. Patients were treated with weekly EEPFL therapy (etoposide 40, epirubicin 10, cisplatin 25, 5-fluorouracil 2200 and leucovorin 120 mg/m2 ). Response, survival and toxicity were evaluated. RESULTS: From April 1997 to April 1999, six patients were included in this study. All patients received EEPFL chemotherapy. Clinical and laboratory evidence of acute DIC stabilized quickly after starting chemotherapy. Four patients showed a partial response, one stable disease and one progressive disease. The toxicity was mild and well tolerated. Median survival was 28 weeks (12, 14, 26, 30, 30 and 32 weeks). All patients suffered from a relapse of DIC after initial successful control and died within 30 days of clinical and laboratory evidence of acute DIC relapse. CONCLUSION: EEPFL therapy is an effective chemotherapy regimen for patients with advanced gastric cancer associated with acute DIC. The prognosis is poor if the DIC relapses after the initial successful control.

Acute Disease↗
PubMed1993

The effect of two-domain tissue factor pathway inhibitor on endotoxin-induced disseminated intravascular coagulation in rabbits.

Disseminated intravascular coagulation (DIC) is a common complication in sepsis, and may result from endotoxin-induced exposure of tissue factor on the surface of monocytes and endothelial cells. Tissue factor pathway inhibitor (TFPI) is a factor Xa-dependent feedback inhibitor of the tissue factor-factor VIIa complex. In the present study the effect on DIC of a two-domain TFPI analogue (2D-TFPI), consisting of the first two Kunitz domains of TFPI but lacking the third domain, was tested. DIC was induced in rabbits by two intravenous bolus injections of endotoxin from Escherichia coli (10 and 50 micrograms/kg) 24 h apart. Simultaneously with the last endotoxin injection an infusion of 2D-TFPI (0, 0.3, 1.0 or 3.0 mg/kg/h) was given. Blood samples were obtained at 0 h, 24 h and 31 h. At 31 h the animals were sacrificed and the kidneys were submitted to histological examination. The degree of fibrin deposition in glomeruli was scored blindly using an arbitrary scale from 0 to 3. Between 24 and 31 h the group receiving endotoxin alone showed a significant decrease in platelet count (65%), plasma fibrinogen (41%), antithrombin III (25%), and factor VIII (63%), and a significant prolongation of the aPTT (14%). Furthermore, massive fibrin deposition was detected in the renal glomeruli at 31 h. Infusions of 2D-TFPI inhibited all the endotoxin-induced changes in a dose-dependent manner. In conclusion, the data demonstrate that inhibition of the TF/FVIIa complex by infusion of 2D-TFPI significantly counteracts endotoxin-induced coagulopathy in rabbits, and might thus be an attractive drug for treatment of endotoxin-induced DIC in humans.

Animals↗
PubMed1983

[Morphologic aspects of intravascular disseminated coagulation. Apropos of 100 cases].

The authors report a morphological study of one hundred cases of disseminated intravascular coagulation (D.I.C.) of various origins. In each case laboratory findings demonstrated an authentic consumption coagulopathy. In all cases organ biopsies were performed either in vitro (rarely), or mainly immediately after death or at autopsy. Optic microscopy was performed for all of them (3 stains were chosen: hemalum eosin saffron, Mallory's phosphotungstic acid hematoxylin stain, P.A.S.). For a smaller number of cases ultrastructural microscopy and immunofluorescence were performed. As far as microscopic findings are concerned, the authors insist particularly upon intravascular microthrombi (fibrinous type and hyalin type). Haemorrhages and particularly necrosis, because of multiple origin, are not detailed. The repartition of these microthrombi is particularly detailed (in connection with the different organs, etiologies, clinical and/or biological findings, treatments). A review of literature is reported.

Adolescent↗
PubMed1994

Increased plasma free gamma carboxyglutamic acid levels during deep vein thrombosis and intravascular disseminated coagulation.

Gammacarboxyglutamic acid (gla) is a non essential amino acid synthesized in presence of vitamin K, predominantly found in coagulation and bone proteins. In 14 cases of deep vein thrombosis and in 11 cases of disseminated intravascular coagulation, compared to 19 normal subjects and 9 patients hospitalized for leg pain, free plasma gla levels were found significantly elevated (respectively 372 +/- 244 and 559 +/- 361 versus 146 +/- 34 and 120 +/- 40 pmol/mL). In six paired plasma and serum, gla levels were similar. These results suggest an involvement of blood coagulation in gla generation with need of a catabolism of the activated factors. A significant decrease was noticed during vitamin K antagonist therapy and liver disease, both instances in which the synthesis of gla containing coagulation factors is affected. During hepatocellular carcinoma with elevated desgamma carboxyprothrombin, gla was found normal, denying an global impairement of the vitamin K metabolism.

1-Carboxyglutamic Acid↗
PubMed1984

Microvascular alterations in thrombin-induced experimental disseminated intravascular coagulation in the dog.

Disseminated intravascular coagulation is often characterized by organ failure and bleeding. By use of light microscopy, previous studies have shown extensive fibrin deposition in vessels. However, quantification of fibrin deposition using ultrastructural methods has not been reported. In this study dogs were infused with thrombin, and disseminated intravascular coagulation developed. Using a blinded morphometric analysis method, we observed deposition of fibrin in nearly half of the microvascular vessels. Such deposition probably accounts at least for part of the organ dysfunction. Almost half the vessels also had altered endothelial structure including thinning of the endothelial membrane, formation of extremely thin spots, fenestrations, and even a few ruptured areas. These findings at least in part explain the extravasation of blood in disseminated intravascular coagulation.

Animals↗
PubMed1993

Disseminated intravascular coagulation: pathophysiology, diagnosis, and treatment.

Disseminated intravascular coagulation is a frequent finding in critically ill patients, and may be diagnosed in the majority of patients with Gram-negative sepsis. Tissue damage may result from intravascular thrombosis, and disseminated intravascular coagulation is an underestimated causal factor in the pathogenesis of organ failure in sepsis. The diagnosis of disseminated intravascular coagulation is difficult, as the initial coagulation process that leads to thrombosis is counteracted by fibrinolytic responses, that in the context of ongoing consumption of clotting factors may result in an overwhelming bleeding tendency. Hence, depending on underlying disease, and the time at which the patient is evaluated, different laboratory results may be obtained. The treatment of disseminated intravascular coagulation is even more challenging than its diagnosis. No well-designed, controlled clinical trials exist that form a basis for rational treatment decisions. Treatment frequently needs to be individualized, and rapid adjustments may be necessitated by the course of the disease. Nonetheless, we believe that recent insights in the pathophysiology of disseminated intravascular coagulation, in particular concerning the role of the extrinsic coagulation pathway, provide ground for some optimism concerning future therapeutic options.

Anticoagulants↗
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↗
PubMedDate not supplied

Successful initial treatment with weekly 24-hour infusion of 5-fluorouracil and leucovorin in a rectal cancer patient with acute disseminated intravascular coagulation.

Cancer-associated acute disseminated intravascular coagulation is rare in colorectal cancer, but is rapidly fatal when present. We present a case of a 79-year-old male who developed acute disseminated intravascular coagulation one month after receiving Hartmann's procedure for his rectal cancer. Peripheral blood showed leucoerythroblastosis while marrow carcinomatosis was noted by bone marrow examination. Prompt chemotherapy with weekly 24-h infusion of 5-fluorouracil and leucovorin were administered and the acute disseminated intravascular coagulation gradually resolved after 2 cycles of treatment. A total of 10 cycles of weekly chemotherapy were administered. The patient died of pneumonia on the 83rd day after diagnosis of disseminated intravascular coagulation without evidence of acute disseminated intravascular coagulation and tumor progression. We suggest that if acute disseminated intravascular coagulation developed after surgery for rectal cancer, the cancer-related acute disseminated intravascular coagulation should be taken into consideration. The immediate administration of chemotherapy may save the patient in time.

Adenocarcinoma↗
PubMed1993

Disseminated intravascular coagulation with leukemia patients.

Disseminated intravascular coagulation (DIC) is a perplexing syndrome that involves both clot formation and bleeding. The management of this syndrome for leukemia patients is especially difficult because of the abnormal coagulation parameters already present in this population. The purpose of this article is to describe normal blood coagulation physiology and the pathophysiology of DIC, and identify appropriate nursing diagnoses and interventions for the leukemia patient with DIC.

Adult↗
PubMed1983

The effects of defibrinogenation with batroxobin on endotoxin-induced disseminated intravascular coagulation in rats.

Experimental disseminated intravascular coagulation (DIC) can be induced by a 4-hr sustained infusion of endotoxin at a dose of 100 mg/kg in rats. This experimental model of DIC in rats was used to study the effects of defibrinogenation with batroxobin against DIC. One hour before the infusion of endotoxin, 200 batroxobin unit (BU)/kg of batroxobin was injected intraperitoneally. Immediately after the injection, fibrinogen level markedly decreased and fibrinogen and fibrin degradation products increased. Prothrombin time and partial thromboplastin time were also prolonged. Blood counts, platelet counts and hematocrit level only showed a slight decrease after the injection. The preventive effect against DIC was noted by the partial inhibition of the fall in the platelet counts and lessened number of renal glomeruli with fibrin thrombi, in the rats treated with 200 BU/kg of batroxobin 1 hr before the infusion of endotoxin (100 mg/kg/4 hr). From these results, it was shown that fibrinogen metabolism plays an important role in the DIC state.

Animals↗
PubMed1999

Dissecting aortic aneurysm complicated with acute disseminated intravascular coagulation: case report.

Acute disseminated intravascular coagulation (DIC) is a rare complication of aortic aneurysm with or without dissection. We describe an 88-year-old man who presented with severe hemorrhagic diathesis and a pulsating abdominal mass. An abdominal computed tomography (CT) scan revealed a dissecting abdominal aortic aneurysm with thrombus formation, and his coagulation profile showed the features of acute DIC. After he had received blood component therapy, including fresh frozen plasma and cryoprecipitate concentrates, and intravenous heparin infusion (10,000 U/day), the bleeding diathesis and coagulopathy improved. An aneurysmectomy was performed smoothly without excessive bleeding. Coagulation parameters returned to normal after surgery. Dissecting aortic aneurysm should be considered as a possible etiology of acute disseminated intravascular coagulation, even it occurs in rare situations. Surgical intervention is still the main strategy to normalize coagulopathy. Bleeding diathesis must be corrected before surgery in order to prevent massive intraoperative bleeding.

Acute Disease↗