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PubMed1980

Disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) is a clinico-pathological syndrome of variable expression, resulting from uncontrolled simultaneous activation of the coagulation and fibrinolytic systems. DIC can be initiated in a variety of different ways. Additional studies are needed to determine the importance of vascular endothelial damage, hemodynamic alterations and the role of naturally occurring inhibitors of hemostasis. Progressive increase in our understanding of the mechanisms involved in triggering DIC will improve our therapeutic measures in the rational management of these patients. Absolutely essential in the successful management of patients with DIC is identification and control of the underlying illness.

Disseminated Intravascular Coagulation↗

PubMedDate not supplied

Trombocytopenia: one of the markers of disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) is a complication of a variety of severe underlying diseases and a contributing factor in multi-organ failure and death. DIC is diagnosed on the basis of clinical findings (organ failure, bleeding) and laboratory abnormalities. The laboratory data include (repeated) measurements of platelet count and global clotting tests, to which more specific and sensitive tests for activated coagulation are added. The focus of this paper is on thrombocytopenia (platelet count < 100 x 103/microl) as a marker in DIC. First, in patients with suspected DIC it is imperative to consider alternative causes of thrombocytopenia,such as related to heparin use (heparin induced thrombocytopenia II) or thrombocytopenic purpura. Second, the observation of thrombocytopenia in relation to DIC should be interpreted as a marker of advanced or overt DIC and not as an early indicator. According to recommended guidelines measurements of platelet counts should always be coupled to a panel of coagulation markers and not be used as single marker of DIC (or other syndromes). In general, thrombocytopenia should not trigger platelet transfusions except in patients with severe bleeding complications.

Disseminated Intravascular Coagulation↗

PubMed2002

The diagnosis of disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) is a syndrome characterized by systemic intravascular activation of coagulation, leading to widespread deposition of fibrin in the circulation. In recent years, the pathogenetic pathways leading to DIC have been largely identified, which could result in more precise diagnostic tests for this disorder. However, the clinical and laboratory diagnosis of DIC may remain difficult, since routinely available tests do not specifically assess ongoing thrombin generation. Molecular markers for activation of coagulation and fibrinogen to fibrin conversion are highly sensitive but also disappointedly aspecific for the diagnosis of DIC. Moreover, these tests are often not available in most settings for daily clinical care. A combination of widely available tests, however, may be helpful in making the diagnosis of DIC, according to a recently developed algorithm.

Algorithms↗

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↗

PubMed2004

Update on the treatment of disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) is 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 treatment of DIC. We focus on the current standard treatment of overt DIC in clinical practice. Moreover, particular attention is made to novel therapeutic strategies, who reflect the important progresses in the understanding of the pathogenesis of this syndrome in the last few years.

Anticoagulants↗

PubMed1993

MRI evaluation and follow-up of bone necrosis after meningococcal infection and disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) is a serious complication of meningococcal septicaemia. It often results in infarction of various tissues namely the skin, adrenal glands, kidneys, brain and, much less commonly, bones. We describe a patient who presented bone lesions after meningococcal septicaemia. In addition to plain radiography and scintigraphy the lesions were evaluated with MRI and have proved to be extensive and still progressive, approximately 18 months after the onset of the disease.

Bacteremia↗

PubMed2005

Mycobacterium tuberculosis inducing disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) can develop infrequently in patients with tuberculosis and has a very high mortality rate. We conducted a retrospective study to evaluate the incidence of tuberculosis-induced DIC and to investigate the clinical manifestation, outcome, and prognostic factors of such patients. From January 2002 to December 2003, all culture-proven tuberculosis patients who developed DIC before starting anti-tuberculosis treatments were selected for this study. Patients who had other clinical conditions or were infected by other pathogens that may have been responsible for their DIC were excluded. Survival analysis was performed for each variable with possible prognostic significance. Our results showed that 27 (3.2%) out of the 833 patients with culture-proven tuberculosis had tuberculosis-induced DIC with a mortality rate of 63.0%. The most common clinical manifestations were fever (63.0%) and multiple patches of pulmonary consolidation (59.3%). Seven (25.9%) patients had disseminated tuberculosis. Twelve (44.4%) developed acute respiratory distress syndrome and three (11.1%) were associated with hemophagocytosis. Twenty-four (88.9%) patients had findings that were unusual for an acute bacterial infection, such as positive acid-fast smear, miliary pulmonary lesions, lymphocytotic exudative pleural effusion, and mediastinal lymphadenopathy. Early anti-tuberculosis treatment significantly improved survival. In conclusion, tuberculosis can cause DIC. Patients with non-miliary, non-disseminated tuberculosis could also develop the rare clinical manifestation. Since the prognosis was very poor in patients not treated at an early stage, a high index of suspicion is required, especially in those with clinical findings suggestive of tuberculosis.

Adult↗

PubMedDate not supplied

Pedal manifestations of disseminated intravascular coagulation.

Disseminated intravascular coagulation is a complex hemostatic imbalance associated with many disease states. The potentially lethal systemic consequences of this disease mandate that the podiatric physician obtain a complete detailed history in addition to proceeding with appropriate consultations from other specialties. If haste is utilized and surgical intervention is undertaken without careful consideration, a potentially fatal situation may ensue. A comprehensive case report highlighting the pedal presentation and complications, and an overview of this disease process are presented.

Aged↗

PubMed2000

Management of disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) is a complex condition in which diffuse clotting and profuse hemorrhaging occur simultaneously. It is a serious, often fatal, condition that is estimated to occur in approximately 10% of all patients diagnosed with cancer. No single laboratory test is available that is absolutely diagnostic for DIC; however, several laboratory results, combined with certain clinical findings, will support the diagnosis. Despite the lack of a standardized protocol for clinical management, aggressive medical and nursing care can play a prominent role in the clinical outcome of the patient with DIC.

Anticoagulants↗

PubMed1997

A selective pulmonary thrombosis associated with sepsis-induced disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) is a pathologic condition associated with critical illnesses, including sepsis. Recent studies have suggested that endogenous cytokines and leukocytes are involved in major roles of its pathophysiology. We report a case of sepsis-induced DIC due to pneumonia that was associated with diffuse and selective thrombosis in pulmonary arteries, yielding to sudden death from pulmonary massive embolism. This report suggests that the selective and lethal pulmonary thromboembolism progresses under the standard therapies in sepsis-induced DIC.

Adult↗

PubMed1985

Disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) is not uncommon in the obstetric patient, but DIC of sufficient severity to be of clinical importance is unusual. Treatment of DIC is directed primarily at its cause. Replacement of depleted blood components with packed red blood cells, fresh frozen plasma, cryoprecipitate, and platelets is sometimes required for treating hemorrhage. Heparin should be used only rarely, and only to help control life-threatening hemorrhage because DIC is refractory to vigorous and adequate blood-component therapy. With careful planning of treatment, adherence to a few general principles, and the combined approach of an obstetrician and a coagulationest, fatalities and major morbidity should be rare.

Abruptio Placentae↗

PubMed2003

Diagnosis and treatment of disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) is a complex clinical syndrome with activation of the procoagulant and fibrinolytic systems along with inhibitor consumption. We discuss regarding the controversies in diagnosis and management of DIC. Bleeding is a more common manifestation of DIC but most of the morbidity and mortality of DIC is due to microvascular thrombosis. Routinely performed tests for DIC such as platelet count and prothrombin time may be normal in chronic DIC. There is no single test that would diagnose DIC, however, estimation of D-dimer appears to be the most sensitive and specific test. Therapy of DIC aims at treating the primary cause. Fresh frozen plasma and platelet concentrates are recommended only in bleeding patients and have the potential risk of adding procoagulant material to the already activated procoagulant system. Role of heparin and antithrombin in patients with sepsis and DIC is discussed.

Disseminated Intravascular Coagulation↗

PubMed1994

Plasma levels of soluble fibrin in patients with malignancy-associated disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) is one of the most critical complications of malignant diseases. It is conventionally diagnosed by a decrease in platelets and an increase in fibrin/fibrinogen degradation products (FDP). Recently, an immunological assay was developed that can directly quantify the amount of soluble fibrin (SF) formed in the blood. This study examined this assay system in the diagnosis of DIC and found that it is a good indicator of both fibrin formation and of DIC. Plasma levels of SF correlated well with the DIC score, which is determined according to the 'DIC Scoring Guideline' proposed by the DIC Study Group under the Japanese Ministry of Public Welfare in 1988. It also correlated well with the serum levels of FDP. Normal values of plasma SF ranged between 0 and 9.50 micrograms/ml. Interestingly, values of SF in females tended to increase with age, for reasons that are not yet determined.

Adolescent↗

PubMed1997

Expression of tissue factor and tissue factor pathway inhibitor in rats lungs with lipopolysaccharide-induced disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) is a frequent complication of endotoxin shock, and modulation of endothelial cell hemostatic properties has been proposed to play an important role in its onset. We examined the in vivo expression of tissue factor (TF) and TF pathway inhibitor (TFPI) in rat lungs of a lipopolysaccharide (LPS)-induced DIC model. Light and electron microscopic studies showed that fibrin-rich thrombi were present in the pulmonary microvasculature 3 hours after intraperitoneal injection of LPS (7.5 mg/kg) and increased in number at 6 hours. In an immunohistochemical study, an increase in number of monocytes in the microvasculature was observed after LPS injection, and many of these cells (> 90%) were positive for TF antigen. However, no TF expression in endothelial cells was detected. Pulmonary endothelial cells showed positive reaction for TFPI antigen before LPS injection, but TFPI-positive endothelial cells markedly decreased in number after LPS injection. mRNA expression of TF increased and that of TFPI decreased in the lung tissue 3 and 6 hours after LPS injection. High values of TF activity were detected in the lung tissue and plasma, whereas TFPI activities decreased after LPS injection. These results indicate that imbalance between TF and TFPI, overexpression of TF, and underexpression of TFPI in the lung may contribute to thrombus formation in this LPS-induced DIC model.

Animals↗

PubMed2001

Fibrin degradation products, fibrin monomer and soluble fibrin in disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) is characterized by activation of hemostasis and fibrinolysis resulting in the formation of thrombin and plasmin, and the characteristic effects of these enzymes on plasma fibrinogen can be useful in diagnosis. Thrombin cleaves fibrinopeptides from fibrinogen, forming fibrin monomer that rapidly polymerizes to form a clot. Small amounts can circulate in plasma as "soluble fibrin," which may have a complex composition and include fibrinogen and a variable amount of cross-linking. Plasmic degradation of cross-linked fibrin forms a heterogeneous group of degradation products reactive in assays for D-dimer, and their levels provide a measure of the amount of fibrin formation and lysis. Caution should be exercised in comparing quantitative results using different assays because of problems with standardization and variable reactivity with different molecular forms. Marked elevations of fibrin(ogen) degradation products are a constant finding in experimental animal models of DIC. In human models of DIC resulting from endotoxin infusion, D-dimer is elevated early and high levels persist, reflecting lysis of microvascular fibrin deposits. Elevated levels of D-dimer and soluble fibrin are very sensitive for the diagnosis of DIC, and a normal level has a high negative predictive value. Serial monitoring of soluble fibrin or D-dimer assays may be of value in evaluating the response to therapy and possibly in identifying at-risk patients.

Animals↗

PubMed2004

Treatment effects of drotrecogin alfa (activated) in patients with severe sepsis with or without overt disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) is a serious condition associated with sepsis. Clinical management of DIC is hampered by lack of clear diagnostic criteria. The International Society on Thrombosis and Haemostasis (ISTH) has proposed a diagnostic scoring algorithm for overt DIC based on routine laboratory tests. The objective was to assess a modified version of the ISTH scoring system and determine the effect of drotrecogin alfa (activated) (DrotAA, recombinant human activated protein C) on patients with DIC. The large database from the PROWESS clinical trial in severe sepsis was retrospectively used to assess a modified ISTH scoring system. Baseline characteristics and treatment effects of DrotAA were evaluated. At baseline, 29% (454/1568) of patients had overt DIC. Overt DIC was a strong predictor of mortality, independent of APACHE II score and age. Placebo-treated patients with overt DIC had higher mortality than patients without (43 vs. 27%). DrotAA-treated patients with overt DIC had a trend towards greater relative risk reduction in mortality than patients without (29 vs. 18%, P = 0.261) but both groups had greater relative risk reduction than placebo-treated patients. Serious bleeding rates during DrotAA infusion in patients with and without overt DIC were slightly increased (P = 0.498), compared with placebo, while clinically overt thrombotic events during the 28-day period were slightly reduced (P = 0.144). Modified ISTH overt DIC scoring may be useful as an independent assessment for identifying severe sepsis patients at high risk of death with a favorable risk/benefit profile for DrotAA treatment. Patients without overt DIC also received significant treatment benefit.

Adult↗

PubMed2006

Recent acquisitions in the pathophysiology, diagnosis and treatment of disseminated intravascular coagulation.

Disseminated intravascular coagulation (DIC) is a disorder characterized by both acute generalized, widespread activation of coagulation, which results in thrombotic complications due to the intravascular formation of fibrin, and diffuse hemorrhages, due to the consumption of platelets and coagulation factors. Systemic activation of coagulation may occur in a variety of disorders, including sepsis, severe infections, malignancies, obstetric or vascular disorders, and severe toxic or immunological reactions. In this review, we briefly report the present knowledge about the pathophysiology and diagnosis of DIC. Particular attention is also given to the current standard and experimental therapies of overt DIC.

Journal Article↗

PubMed1996

[Disseminated intravascular coagulations].

Disseminated intravascular coagulation (DIC) syndromes can be defined as the formation of fibrin deposits within the microcirculation, occurring in definite clinical situations. Their biological counterpart is a consumption coagulopathy. The clinical profiles of DIC have been well known for decades, are multiform and range from latency to overwhelming haemorrhagic diatheses, including also characteristic but rare situations, such as purpura fulminans, acral cyanosis and pictures resembling thrombotic thrombocytopenic purpura or haemolytic-uraemic syndrome. Biological tests of DIC show a consumption coagulopathy, displayed on the standard haemostasis sheet; along with signs of paracoagulation and/or of secondary fibrinolysis (FDP). New tests have recently been introduced: D-dimers are specific and sensible; Antithrombin-III, protein C and alpha 2-antiplasmin also can sometimes be useful. The knowledge of the pathophysiology of DIC has made advances with passing years. Fibrin deposits may be non-occlusive, and indeed they are swiftly removed by a secondary fibrinolysis. Except in very rare situations, such as those leading to a cortical renal necrosis, and perhaps in some ARDS, there is little evidence relating DIC to organ failure syndromes. Moreover, there is no clear relationship between the severity of the consumption coagulopathy and the prognosis. For instance, the mortality is much lower in abruptio placentae, where the coagulopathy is very severe, than in septic shock, where it is usually moderate. In septic shock, the disorders of haemostasis were related initially to a platelet activation, then to an activation of the contact system (releasing kinins and triggering complement cascade), and nowadays to the activation of the extrinsic coagulation system. The treatment of DIC is mainly the treatment of its cause. Indications for heparin therapy should be strictly limited to a few exceptional circumstances. When haemorrhagic diathesis threatens, FPC and/or platelet transfusion may be indicated. Aprotinin can be useful in rare cases of overwhelming secondary fibrinolysis. Trials with antithrombin-III or C1-esterase inhibitors are in progress.

Blood Coagulation↗