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PubMed2000

[Disseminated intravascular coagulation].

Disseminated intravascular coagulation is characterised by systemic activation of blood coagulation, resulting in formation of intravascular thrombi and impaired organ perfusion. Simultaneously, the ongoing consumption of platelets and coagulation factors may lead to bleeding. Disseminated intravascular coagulation is seen in septicaemic infections, trauma, malignancies, obstetrical complications, vascular diseases, toxic and immunological reactions. In summary, the systemic deposition of fibrin is caused by enhanced thrombin generation, simultaneous depression of physiological anticoagulant mechanisms and diminished fibrin degradation due to inhibition of fibrinolysis. The increased insight into the pathogenesis of disseminated intravascular coagulation provides a solid basis for development of improved management strategies for patients with this complication. Therapy may include anticoagulants, platelet and plasma transfusion, concentrates of coagulation inhibitors and antifibrinolytic agents.

Anticoagulants↗
PubMed1995

Disseminated intravascular coagulation.

Disseminated intravascular coagulation is the result of a severe underlying disorder that initiates massive activation of the coagulation system. It is always a symptom of the underlying disorder. These disorders may be as varied as meningococcemia and abdominal aortic aneurysm. Disseminated intravascular coagulation is a clinical diagnosis. Once the clinical impression has been considered, a small number of readily available tests will substantiate the diagnosis. Further testing is probably not necessary and certainly not cost-effective. Therapy for disseminated intravascular coagulation requires 1) the correction of the underlying problem, either by drainage of an abscess for sepsis, evacuation of the uterus in an obstetric catastrophe, or treatment of septicemia with antibiotics; and 2) the concomitant restoration of the circulatory system, perfusion, blood pressure, and electrolyte balance. Other forms of therapy are available but are quite secondary to these two. Success depends on the ability to recognize and correct the cause.

Anticoagulants↗
PubMed1994

Current management of disseminated intravascular coagulation.

Disseminated intravascular coagulation is a complex process seen in a wide variety of clinical disorders. The oncology patient may develop this syndrome either as a result of the neoplasm itself or of the treatment of the neoplasm. An understanding of the pathophysiology of disseminated intravascular coagulation is essential for diagnosis and treatment. Diagnosis is accomplished by correlating clinical and laboratory data. Treatment remains controversial, but reversal of the triggering mechanism is the single most important factor in successful treatment. Other interventions, including the use of heparin, antithrombin III, and hirudin, are being studied. Much remains to be understood about disseminated intravascular coagulation, and controlled clinical trials are needed to define optimal treatment.

Antithrombin III↗
PubMed1998

[The paradox of disseminated intravascular coagulation].

Disseminated intravascular coagulation (DIC) is an abnormal extension of a coagulation process normally limited in time and space. DIC results from the release of free thrombin in circulating blood, as thrombin synthesis and inactivation mechanisms non longer function properly. In addition to microthrombosis, acute DIC may lead to haemorrhage related to activation of the coagulation process. According to the disease aetiology, emergency treatment may become a top priority, in case of haemorrhage, shortage of platelets and coagulation factors related to increased use of these blood components requires replacement treatment with infusion of platelets and fresh frozen plasma. As treatment of the procoagulation process, heparin should not be recommanded in acute DIC with haemorrhage. Based on rational theoretical data, current evaluation of antithrombin therapy is in progress.

Blood Coagulation↗
PubMed2003

Disseminated intravascular coagulation.

Disseminated Intravascular Coagulation (DIC) is an acquired syndrome representing a hypercoagulable state, haemorrhagic symptoms and multiple organ failure. The clinical relevance of this syndrome is complicated since there is no established way of diagnosing DIC and it is difficult to distinguish whether clinical features are attributable to the underlying disease or DIC. Experimental studies, based on models of gram-negative sepsis and the Generalized Shwartzman Reaction, show that DIC is characterized by strongly enhanced inflammatory activity, activated coagulation and impaired fibrinolysis. In this review we propose that activated neutrophils play a pivotal role in the pathophysiology of DIC, particularly by contributing to inflammation and vascular injury. Additionally, a distinct role for granulocytes in fibrinolysis has also been suggested. Although the underlying procoagulant pathways of DIC and the important role of tissue factor have been unravelled, therapeutic interventions counteracting the mediators of these pathways proved mainly unsuccessful (with the positive exception of activated protein C). Dissecting the molecular interactions at the onset and progression of DIC might therefore help to elucidate the fundamental consequences of DIC, possibly contributing to better diagnostic tools and more effective therapeutic options.

Blood Coagulation↗
PubMedDate not supplied

Idiopathic chronic disseminated intravascular coagulation.

Disseminated intravascular coagulation, whether acute or chronic is usually associated with an underlying causative condition. In this case chronic disseminated intravascular coagulation persisted in one 79 year old man for 3 years with no detectable underlying cause.

Aged↗
PubMed2001

Regulatory role of cytokines in disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) can complicate a number of diseases. DIC in the setting of sepsis is considered to result from strong activation of the coagulation system and concurrent inhibition of fibrinolysis and other anticoagulant pathways. Cytokines have been implicated as important mediators in these hemostatic alterations. This article summarizes recent insights into which cytokines are likely to be involved in the procoagulant response to systemic infection.

Animals↗
PubMed2003

Etiopathophysiology of disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) involves activation of clotting as well as fibrinolytic pathways. Thrombosis from thrombin release results in end-organ damage, whereas consumption of coagulation factors results in bleeding. Sepsis is the commonest cause of DIC. The consumption of antithrombin in sepsis abrogates its anti-inflammatory role and so its low level is a poor prognostic marker in sepsis. The increased release of plasminogen activator inhibitor-1 (PAI-1) as seen in sepsis decreases fibrinolysis and promotes increased microvascular thrombosis. Here, we discuss the role of inhibitors of coagulation, cytokines, kinins, complement and vasoactive peptides in DIC.

Blood Coagulation↗
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↗
PubMed1998

Current drug treatment strategies for disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) can be caused by a variety of diseases. Experimental models of DIC have provided substantial insight into the pathogenesis of this disorder, which may ultimately result in improved treatment. Disseminated coagulation is the result of a complex imbalance of coagulation and fibrinolysis. Simultaneously occurring tissue factor-dependent activation of coagulation, depression of natural anticoagulant pathways and shutdown of endogenous fibrinolysis all contribute to the clinical picture of widespread thrombotic deposition in the microvasculature and subsequent multiple organ failure. Cornerstone for the treatment of DIC is the optimal management of the underlying disorder. At present, specific treatment of the coagulation disorders themselves is not based on firm evidence from controlled clinical trials. Plasma and platelet transfusion are used in patients with bleeding or at risk for bleeding and low levels of coagulation factors or thrombocytopenia. The role of heparin and low molecular weight heparin is controversial, but their use may be justified in patients with active DIC and clinical signs of extensive fibrin deposition such as those with meningococcal sepsis. There is some evidence to indicate that low molecular weight heparin is as effective as unfractionated heparin but may be associated with a decreased bleeding risk. Antithrombin III (AT III) replacement appears to be effective in decreasing the signs of DIC if high doses are administered, but effects on survival or other clinically significant parameters are at best uncertain. If AT III supplementation is used, the dosage should be selected to achieve normal or supranormal plasma levels of 100% or higher. Results of studies on protein C concentrate, thrombomodulin or inhibitors of tissue factor are promising, but the efficacy and safety of these novel strategies remains to be established in appropriate clinical trials.

Anticoagulants↗
PubMedDate not supplied

Understanding disseminated intravascular coagulation.

Disseminated intravascular coagulation is associated with a high mortality rate, with patient outcomes largely dependent upon swift recognition and appropriate management of events. This article provides a basic overview of the condition, and its pathophysiology, diagnosis, treatment and nursing management, so that effective intervention may be implemented, maximising the chances of patient recovery.

Blood Coagulation Tests↗
PubMed1992

Massive pulmonary embolism presenting as disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) can be defined as evidence of activation of the coagulation mechanism resulting in proteolysis of fibrinogen by thrombin and plasmin and an acute thrombocytopenia. The association of pulmonary embolism (PE) with DIC has recently been reported but in reviewing recent textbooks of hematology, there is no mention of PE as a cause of DIC. Clinicians need to be made aware of this association since it affects the patient who is thought to be autoanticoagulated as well as the patient who has DIC of unknown cause. PE needs to be included in the differential diagnosis of an autoanticoagulated state and in DIC of unknown etiology. In both instances the recommended treatment is full-dose intravenous heparin therapy.

Aged↗
PubMed1996

Aortic aneurysm-induced disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) may result in hemorrhagic and thrombotic complications and is rarely associated with stable abdominal aortic aneurysms. In a retrospective review of our experience over the past 5 years, we identified only two instances of DIC-associated abdominal aortic aneurysms among a total of 67 patients who were operated on for asymptomatic aneurysms. In the first patient with DIC induced by abdominal aortic aneurysm, consumptive coagulopathy and a bleeding diathesis developed. The second patient's course was complicated by consumptive coagulopathy and migrating thrombophlebitis. In both instances coagulopathy resolved after surgical intervention. In this report we briefly discuss the pathogenesis and laboratory diagnosis of aneurysm-associated DIC and review current management strategies.

Aged↗
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↗
PubMedDate not supplied

Trauma, sepsis, and disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) was first observed clinically in a case of sepsis following severe trauma. It was postulated that the observed clotting defect and bleeding were due to the using up of clotting factors in an episode of intravascular clotting. It was also postulated that the multiple organ failure observed was due to obstruction of the microcirculation of the organs by microclots. Evidence for this process was worked out in many animal studies. It was then postulated that if these microclots could be lysed before organ necrosis was produced, organ failure could be prevented. This prevention was shown to be possible in animals. It was then tried in humans using plasminogen activators, and the approach was found to be effective. Using a low dose of plasminogen activator over a 24-hour period caused no changes in the coagulation profile or bleeding.

Adult↗
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↗
PubMed2003

[Disseminated intravascular coagulation].

Disseminated intravascular coagulation (DIC) is an acquired syndrome characterized by systemic formation of microthrombi and fibrin deposition in the vasculature. Cancer is one of the leading cause of DIC, which often complicates bleeding tendency and organ dysfunction. Even though DIC therapy is expectant, it is still important, since the bleeding tendency limits the quality of patients' life remarkably. Heparin, low molecular weight heparin, danaparoid, protease inhibitors for coagulation factors and antithrombin III are the choices for DIC. However, since the selection of the drugs is different depending on the basal disease, it is important to understand the pathophysiology of the individual situation. In general, protease inhibitors is recommended for 'fibrinolysis dominant DIC' like DIC associated with leukemia and terminal stage solid cancer, in contrast, danaparoid and antithrombin III are the first choice for 'coagulation dominant DIC' like sepsis. Supplement of concentrated platelets and fresh frozen should be limited for the patients whose primary disease can be controlled.

Disseminated Intravascular Coagulation↗