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PubMed1988

[Evaluation of several parameters of coagulation in liver cirrhosis: disseminated intravascular coagulation or pseudo-disseminated intravascular coagulation?].

Reports in the literature on the difficulty of differential diagnosis between Disseminated Intravascular Coagulation (DIC) Pseudo-DIC and Primary Fibrinolysis (PF) in patients with liver disease, stimulated a study of various coagulation parameters (PT, PTT, Platelets, Fibrinogen, FDP) in 28 cirrhotic patients. The study confirmed reports in the literature on the high incidence of circulating FDP among liver disease patients. The vital role these play in maintaining alterations in haemostasis means that cirrhosis cases must be approached with extreme caution, avoiding any therapeutic or instrumental procedure liable to worsen the already disturbed coagulation pattern in such patients.

Adult↗
PubMed1999

Monoclonal antibody specific for tissue factor pathway inhibitor-factor Xa complex: its characterization and application to plasmas from patients with disseminated intravascular coagulation and pre-disseminated intravascular coagulation.

Tissue factor pathway inhibitor (TFPI), a Kunitz-type protease inhibitor with three tandem inhibitory domains (K1, K2 and K3), inhibits the initial reactions of the extrinsic blood coagulation pathway through its K1 and K2 domains. We prepared and characterized a monoclonal antibody (Mab8-1) against TFPI-factor Xa (TFPI-Xa) complex. The reactivities of Mab8-1 toward TFPI-Xa complex, TFPI without C-terminal (TFPI-C)-Xa complex, K1K2-Xa complex and K2K3-Xa complex were examined using a surface plasmon resonance analysis (Biacore). The Biacore system allowed a quantitative analysis of antibody-antigen interaction, in real time, from which the association and dissociation rate constants could readily be obtained. The bindings of Mab8-1 to TFPI-Xa complex, TFPI-C-Xa complex and K2K3-Xa complex were each concentration-dependent. However, no binding of Mab8-1 to the K1K2-Xa complex was observed. The binding of Mab8-1 to TFPI or Xa was also not observed. These results suggested that the epitope for Mab8-1 was exposed in the K3 domain of TFPI, which was generated by the conformational change after the formation of TFPI-Xa complex. We then developed an enzyme-linked immunosorbent assay method specific for TFPI-Xa complex using Mab8-1, and we used this assay to measure plasma levels of TFPI-Xa. The normal range assessed from analyses of plasma from 30 normal healthy volunteers was 17.7-66.7 with a mean of 35.5 +/- 11.7 pmol/l. In order to asses the clinical implication of TFPI-Xa complex in the plasma of patients with thrombotic disorders, plasma concentrations were measured in 37 patients with disseminated intravascular coagulation (DIC) caused by a variety of underlying diseases. The TFPI-Xa antigen levels were significantly higher in the patients with DIC (51.9 +/- 21.6 pmol/l) and the 36 patients with pre-DIC (55.1 +/- 20.2 pmol/l) than in the 137 non-DIC patients (37.9 +/- 13.1 pmol/l). In the patients with DIC or pre-DIC, there was no significant correlation between TFPI-Xa complex and the elevated levels of thrombin-antithrombin complex, plasmin-alpha2 plasmin inhibitor complex, D-dimer, soluble fibrin monomer, soluble thrombomodulin or tissue factor. These data indicate that the plasma level of TFPI-Xa seems to be a novel independent molecular marker of DIC and pre-DIC.

Antibodies, Monoclonal↗
PubMed1999

Serum thrombomodulin as a prognostic marker of disseminated intravascular coagulation.

Disseminated intra-vascular coagulation (DIC) is associated with severe bleeding tendency and organ failure, the extent of which is thought to be related to the prognosis of DIC patients. Thrombomodulin (TM) is a high-affinity thrombin receptor on vascular endothelial cells. Clinical importance of soluble TM is still controversy as a diagnostic and prognostic indicator in patients with disseminated intravascular coagulation (DIC). We compared plasma levels of TM with fibrin degradation product (FDP) in patients with DIC through the clinical course. The significant elevation of circulating TM in nonsurvivors with DIC compared with survived patients with DIC(TM 3.1+/-1.52 vs 8.1+/-3.89 FU/ml), as well as FDP (12.9+/-12.12 vs 49.8+/-55.42 microg/ml) but the levels of FDP were not different between the two groups. The measurement of circulating TM was a relatively good prognostic marker of patients with DIC.

Adult↗
PubMed1986

Variant translocation t(8;22) and abnormalities of chromosome 15(q22) and 17(q12-21) in a Burkitt's lymphoma/leukaemia with disseminated intravascular coagulation.

Severe disseminated intravascular coagulation was observed in a patient with Burkitt's lymphoma/leukaemia. Immunological studies on leukaemic blasts from relapsed bone marrow revealed a B-cell phenotype (B4+, B1+, HLA-Dr+, J5+) with membrane bound IgM lambda. Cytogenetic investigation revealed a variant Burkitt's translocation t(8;22)(q24;q11) involving the lambda light chain gene region and abnormalities of chromosomes 15 and 17 with breakpoints at q22 and q12 respectively, similar to those observed in the t(15;17) in acute promyelocytic leukaemia. Transmission electron microscopy of the leukaemic blasts showed crystalline cytoplasmic inclusions which may have had a role in precipitating the disseminated intravascular coagulation.

Adult↗
PubMed2006

Thrombin generation by exposure of blood to endotoxin: a simple model to study disseminated intravascular coagulation.

Pathologic disseminated intravascular coagulation (PDIC) is a serious complication in sepsis. In an in-vitro system consisting of incubation of fresh citrated blood with lipopolysaccharides (LPS) or glucans and subsequent plasma recalcification plasmatic thrombin was quantified. Five hundred microliters of freshly drawn citrated blood of healthy donors were incubated with up to 800 ng/mL LPS (Escherichia coli) or up to 80 microg/mL Zymosan A (ZyA; Candida albicans) for 30 minutes at room temperature (RT). The samples were centrifuged, and 30 microL plasma were recalcified with 1 volume or less of CaCl(2) (25 micromoles Ca(2+)/mL plasma). After 0 to 12 minutes (37 degrees C), 20 microL 2.5 M arginine, pH 8.6, were added. Thirty microliters 0.9 mM HD-CHG-Ala-Arg-pNA in 2.3 M arginine were added, and the absorbance increase at 405 nm was determined. Fifty microliters plasma were also incubated with 5 microL 250 mM CaCl2 for 5, 10, or 15 minutes (37 degrees C). Fifty microliters 2.5 M arginine stops coagulation, and 50 microL 0.77 mM HD-CHG-Ala-Arg-pNA in 2.3 M arginine starts the thrombin detection. The standard was 1 IU/mL thrombin in 7% human albumin instead of plasma. Arginine was also added in the endotoxin exposure time (EET) or in the plasma coagulation reaction time (CRT). Tissue factor (TF)-antigen and soluble CD14 were determined. LPS at blood concentrations greater than 10 ng/mL or ZyA at greater than 1 microg/mL severalfold enhance thrombin generation, when the respective plasmas are recalcified. After 30 minutes EET at RT, the thrombin activity at 12 minutes CRT generated by the addition of 200 ng/mL LPS or 20 microg/mL ZyA is approximately 200 mIU/mL compared to approximately 20 mIU/mL without addition of endotoxin, or compared to about 7 mIU/mL thrombin at 0 minutes CRT. Arginine added to blood or to plasma inhibits thrombin generation; the inhibitory concentration 50% (IC 50) is approximately 15 mM plasma concentration. Endotoxin incubation of blood increases neither TF nor sCD14. This assay allows the study of the hemostasis alteration in PDIC, particularly in PDIC by sepsis. The thrombin generated by blood plus endotoxin incubation and plasma recalcification suggests that the contact phase of coagulation; e.g., triggered by cell components of (phospholipase-) lysed cells such as monocyte or endothelium DNA or phospholipid-vesicles (microparticles), is of primary pathologic importance in sepsis-PDIC. Arginine at plasma concentrations of 10 to 50 mM might be a new therapeutic for sepsis-PDIC.

Arginine↗
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↗
PubMed2000

Novel approaches to the management of disseminated intravascular coagulation.

OBJECTIVE: Disseminated intravascular coagulation (DIC) is a syndrome characterized by systemic intravascular activation of coagulation, leading to widespread deposition of fibrin in the circulation. We addressed the issue of whether there is evidence that this fibrin deposition contributes to multiple organ failure. We also explored the current knowledge on the pathogenesis of DIC and reviewed current and future treatment for DIC. DATA SOURCES: We searched and reviewed published articles on experimental studies of DIC models in animals and clinical studies in patients with DIC. DATA SYNTHESIS: There is ample experimental and clinical evidence that DIC contributes to morbidity and mortality. Recent knowledge on important pathogenetic mechanisms that may lead to DIC has resulted in novel preventive and therapeutic approaches to patients with DIC. Although the trigger for the activation of the coagulation system may vary depending on the underlying condition, it is usually mediated by several cytokines. Thrombin generation proceeds via the (extrinsic) tissue factor/factor VIIa route and simultaneously occurring depression of inhibitory mechanisms, such as antithrombin III and the protein C-protein S system. Also, impaired fibrin degradation, because of high circulating levels of plasminogen activator inhibitor, type 1, contributes to enhanced intravascular fibrin deposition. CONCLUSIONS: Although the cornerstone of DIC management is the specific and vigorous treatment of the underlying disorder, strategies aimed at inhibiting coagulation activation may theoretically be justified. Such strategies have been found to be beneficial in experimental and initial clinical studies. These strategies, which follow from our current understanding of the pathophysiology of DIC, involve inhibition of tissue factor-mediated activation of coagulation or restoration of physiologic anticoagulant pathways by means of the administration of antithrombin concentrate or (activated) protein C concentrate. Although no complete evidence from controlled clinical trials is available for most of the proposed therapeutic interventions, these novel strategies are being studied.

Animals↗
PubMed2001

Disseminated intravascular coagulation (DIC).

Disseminated intravascular coagulation (DIC) is a condition that is seen in critical care areas in association with a number of precipitating conditions. DIC is often described as a paradoxical disease process of concurrent haemorrhage and thrombus formation, resulting in a range of clinical manifestations related to end organ ischaemia. This article will discuss the coagulation cascade as a basis for understanding the aetiology and pathophysiology of DIC. The discourse surrounding medical treatment will be highlighted to enable bedside nurses to understand the divergent orders they may receive from physicians for different patients. Management of the patient experiencing DIC will be approached from a multidisciplinary focus, as well as highlighting the specific nursing considerations and alternatives from an independent focus.

Disseminated Intravascular Coagulation↗
PubMed1997

Novel and diagnostically applicable information from optical waveform analysis of blood coagulation in disseminated intravascular coagulation.

Transmittance waveform is the term applied to the optical profile generated from the process of clot formation on standard coagulation tests run on the MDA-180, a new-generation automated coagulation analyser. In patients with disseminated intravascular coagulation, a characteristically abnormal 'biphasic change' is seen on both the activated partial thromboplastin time and thrombin time waveforms. Increasing steepness of the initial slope on the waveform correlates with clinical deterioration and fulminant progression. Although the mechanism underlying the biphasic appearance remains to be elucidated, its identification provides the diagnostic laboratory with a simple, rapid and robust assay for disseminated intravascular coagulation that can help the clinician with urgent and appropriate therapeutic interventions.

Blood Coagulation↗
PubMedDate not supplied

Quinine-induced disseminated intravascular coagulation.

Recurrent disseminated intravascular coagulation occurred in 3 women after ingestion of quinine tablets for cramp. All had circulating quinine-dependent antibodies to platelets and in 2 there was initial evidence of antibody consumption, with low titres that rose steeply over the next few days and remained high for many months.

Adolescent↗
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↗
PubMed2004

Recombinant activated factor VII in patients with cancer and hemorrhagic disseminated intravascular coagulation.

Hemorrhagic disseminated intravascular coagulation (DIC) associated with the presence of underlying advanced or metastatic tumors are often difficult to control by conventional methods. We report the use of recombinant activated factor VII (rFVIIa) in patients with cancer and bleeding secondary to DIC. A total of 18 patients with cancer met pre-defined criteria for DIC. All patients had failed to respond to transfusion with blood products and treatment of the underlying malignancy prior to the introduction of rFVIIa. The median laboratory data at the time of treatment with rFVIIa were as follows: hemoglobin, 7.7 g/dl; platelets, 54 x 10(9)/l; prothrombin time, 21 s; activated partial thromboplastin time, 41 s fibrinogen, 83 mg/dl; D-dimer, 17 microg/ml; and antithrombin, 32%. The dose of rFVIIa was 90 microg/kg and the median number of doses administered was 5 (range, 3-10). Serial measurements of coagulation parameters were obtained at frequent intervals during treatment with rFVIIa. Of the 18 patients, 15 responded with cessation of bleeding and improvement in coagulation data. The prothrombin time and activated partial thromboplastin time normalized in all responding patients within 24 h of treatment. The median fibrinogen was 214 mg/dl while the median D-dimer was 6 microg/dl at 48 h following the administration of rFVIIa. No thromboembolic complications were observed following rFVIIa. Our data provide evidence that rFVIIa can be used successfully to control the hemorrhagic episodes associated with DIC. Although this type of treatment appears to be safe, close monitoring of the patients is warranted.

Aged↗
PubMed1999

Amniotic fluid embolism and isolated disseminated intravascular coagulation.

PURPOSE: Disseminated intravascular coagulation (DIC) is a well-known complication of an amniotic fluid embolus. However, clinical experience has shown that, in some patients, clinical hemorrhage may be the initial presentation. Mortality in this subset of patients is high. This report describes a patient with a suspected amniotic fluid embolus who survived and in whom the initial presentation was post partum hemorrhage. CLINICAL FEATURES: During the post delivery repair of a fourth degree perineal tear a 29 yr old prima gravida was noted to have excessive vaginal bleeding despite a well contracted uterus. Laboratory investigations revealed a decrease in hemoglobin from 126 g x l(-1) to 86 g x l(-1) and a severe disseminated intravascular coagulopathy (PT 27.5 sec, APPT 149 sec, direct fibrinogen < 0.6 g x l(-1), FDP > 640 g x l(-1)). Treatment included massive blood component therapy and, eventually, total abdominal hysterectomy. The patient subsequently recovered without sequelae. In the absence of any other explanation, the coagulopathy was considered to be secondary to amniotic fluid embolus. CONCLUSION: Amniotic fluid embolus remains an important cause of maternal mortality. Clinical reports, reviews of the literature, and the development of the national registry have all contributed to our understanding of this syndrome. Contrary to earlier beliefs, not all patients present with sudden cardiorespiratory collapse. As the present case illustrates, a less common presentation is the development of an isolated DIC in the peripartum period without antecedent hemodynamic or respiratory instability. Therefore, anesthesiologists must maintain a high index of suspicion for the disorder in order to facilitate early recognition and treatment.

Adult↗
PubMed2001

[Disseminated intravascular coagulation(DIC)].

Disseminated intravascular coagulation (DIC) remains a multifaced syndrome, which may develop with different background and aetiology into venous thromboembolism (mainly chronic, paraneoplastic DIC) or into severe bleeding, factor consumption, thrombocytopenia (i.e. gynaecological acute DIC) or may appear as microthrombotic organ hypoperfusion, organ-failure and necrosis (septic DIC variant). The understanding and consideration of pathogenetic events promotes better identification and interpretation of DIC syndrome and its categories, render more adequate diagnostics and therapy available. The vast majority of new data accumulated in the septic type of DIC, and this general review also tries to put the major emphasis on sepsis-DIC link, laboratory diagnosis and apparent new therapeutic approaches.

Acute Disease↗
PubMed2006

Treatment effects of high-dose antithrombin without concomitant heparin in patients with severe sepsis with or without disseminated intravascular coagulation.

BACKGROUND: Disseminated intravascular coagulation (DIC) is a serious complication of sepsis that is associated with a high mortality. OBJECTIVES: Using the adapted International Society on Thrombosis and Haemostasis (ISTH) diagnostic scoring algorithm for DIC, we evaluated the treatment effects of high-dose antithrombin (AT) in patients with severe sepsis with or without DIC. PATIENTS AND METHODS: From the phase III clinical trial in severe sepsis (KyberSept), 563 patients were identified (placebo, 277; AT, 286) who did not receive concomitant heparin and had sufficient data for DIC determination. RESULTS: At baseline, 40.7% of patients (229 of 563) had DIC. DIC in the placebo-treated patients was associated with an excess risk of mortality (28-day mortality: 40.0% vs. 22.2%, P < 0.01). AT-treated patients with DIC had an absolute reduction in 28-day mortality of 14.6% compared with placebo (P = 0.02) whereas in patients without DIC no effect on 28-day mortality was seen (0.1% reduction in mortality; P = 1.0). Bleeding complications in AT-treated patients with and without DIC were higher compared with placebo (major bleeding rates: 7.0% vs. 5.2% for patients with DIC, P = 0.6; 9.8% vs. 3.1% for patients without DIC, P = 0.02). CONCLUSIONS: High-dose AT without concomitant heparin in septic patients with DIC may result in a significant mortality reduction. The adapted ISTH DIC score may identify patients with severe sepsis who potentially benefit from high-dose AT treatment.

Aged↗