Disseminated Intravascular Coagulation: Experience in a Major Cancer Center

1975 ◽  
Author(s):  
Hamid Al-Mondhiry
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Cancer Center ◽  
Vascular Tumors ◽  
Thrombin Time ◽  
Severe Liver ◽  
Liver Impairment ◽  
Intravascular Coagulation ◽  
Number Of Patients ◽  
Severe Liver Disease ◽  
Precipitating Factor

Disseminated intravascular coagulation (DIC) developed in 89 patients seen at Memorial Sloan-Kettering Cancer Center between 1971 and 1974. Criteria for the diagnosis of DIC wore: 1. Hypofibrinogenemia or > 50% reduction in plasma fibrinogen on serial determinations. 2. Prolonged thrombin time and/or elevated titer of fibrinogen-related material in the serum. 3. Thrombocytopenia not due to drugs or disease. Patients with severe liver disease or uremia were excluded. The patients included 19 with leukemia (17 acute), 3 with multiple myeloma, 15 with lymphoma, 46 with metastatic solid tumors (12 genitourinary, 10 lung, 9 breast, 8 gastrointestinal, 7 miscellaneous), 4 with vascular tumors, and 3 without tumor. Other conditions which might have precipitated or initiated DIC such as gramnegative sepsis (20 patients), mild liver impairment (31 patients), and mucin secreting tumors (4 patients), were also noted. Four patients with vascular tumors, two with leukemia, and one with vasculitis had markedly shortened fibrinogen survival. Bleeding occurred in 75% of the patients and was fatal in 36%. Thromboembolism occurred in 22.5%. Thirteen percent were asymptomatic. Treatment with heparin was helpful in only three of twenty patients. Eighty percent of the patients died within one to over 30 days of the onset of DIC. Post mortem evidence of DIC was present in 18 of 43 autopsies.Results of this study indicate that DIC is a frequent complication of a wide variety of tumors and that its occurrence causes morbidity and mortality in a significant number of patients. Treatment with heparin is of little help unless remission is induced and the precipitating factor(s) are reversed.

Disseminated Intravascular Coagulation

1975 ◽  
Vol 34 (01) ◽  
pp. 181-193 ◽  
Author(s):  
Hamid Al-Mondhiry
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Medical Records ◽  
Lactic Dehydrogenase ◽  
Cancer Center ◽  
Vascular Tumors ◽  
Laboratory Studies ◽  
Intravascular Coagulation ◽  
Serum Lactic Dehydrogenase ◽  
Number Of Patients ◽  
Qualitative Changes

SummaryReview of the coagulation laboratory records and medical records at Memorial Sloan-Kettering Cancer Center over a three year period (1971-1974) revealed 89 patients with disseminated intravascular coagulation (DIC). The diagnosis of DIC was made if laboratory studies showed evidence of quantitative and qualitative changes in fibrinogen and significant thrombocytopenia. The patients included 19 with leukemia (17 acute), 3 with multiple myeloma, 15 with lymphoma, 46 with metastatic solid tumors, (10 lung, 9 breast, 8 gastrointestinal, 12 genitourinary, 7 miscellaneous) 4 with vascular tumors, and 3 without tumor. Other conditions which might have precipitated or initiated DIC such as gram-negative sepsis, liver impairment, or mucin secreting tumors were present in the majority of patients. Bleeding occurred in 75% of the patients and was fatal in 36%. Thromboembolism occurred in 22.5%. Thirteen percent were asymptomatic. Serum lactic dehydrogenase was elevated in over 75 % of the patients at the time of, or subsequent to the occurrence of DIC. Treatment with heparin was helpful in only three of twenty patients. Eighty percent of the patients died within one to over 30 days of the onset of DIC. Post mortem evidence of DIC was present in 18 of 43 autopsies. Results of this study indicate that DIC is a frequent complication of a wide variety of tumors and that its occurrence causes morbidity and mortality in a significant number of patients. Treatment with heparin is of little help unless remission is induced and the precipitating factor(s) are reversed.

The Role of Hageman Factor in Disseminated Intravascular Coagulation Induced by Septicemia, Neoplasia, or Liver Disease

1971 ◽  
Vol 26 (02) ◽  
pp. 325-331 ◽  
Author(s):  
J. W Mason ◽  
R. W Colman
Keyword(s):  
Liver Disease ◽  
Disseminated Intravascular Coagulation ◽  
Plasma Kallikrein ◽  
Severe Liver ◽  
Gram Negative ◽  
Hageman Factor ◽  
Intravascular Coagulation ◽  
Gram Negative Bacteremia ◽  
Severe Liver Disease

SummaryThe human plasma kallikrein system was assayed in patients with disseminated intravascular coagulation (DIC) induced by gram negative bacteremia, neoplasia and severe liver disease. Only the patients with gram negative septicemia showed activation of plasma kallikrein with concomitant depletion of kallikreinogen and kallikrein inhibition. Since the activation of kallikrein is a function of activated Hageman factor, it is suggested that in DIC associated with gram negative septicemia, Hageman factor activation may be involved in the DIC. In DIC associated with neoplasia or liver disease lack of Hageman factor activation should be considered.

scholarly journals Detection of disseminated intravascular coagulation with the help of the conception of constant intravascular microcoagulation

2010 ◽  
Vol 138 (suppl. 1) ◽  
pp. 53-58
Author(s):  
Igor Bokarev ◽  
Ludmila Popova
Keyword(s):  
Blood Coagulation ◽  
19Th Century ◽  
High Mortality ◽  
Disseminated Intravascular Coagulation ◽  
Intravascular Coagulation ◽  
Number Of Patients ◽  
Arteries And Veins ◽  
Exact Diagnosis

The possibility of intravascular blood coagulation existence in the microvascular vessels and capillaries without the presence of a large thrombus in the arteries and veins has been known from the middle of 19th century. It is impossible to know exactly about the prevalence of this pathology, because there is a jumble in terminology that does not help statistics to be exact. One of the reasons of so high mortality from disseminated intravascular coagulation (DIC) is due to the impossibility to always make exact diagnosis, and as ?. Levi thinks it is provoked in the absence of generally accepted idea of DIC syndrome. We investigated these markers and the intensity of intravascular blood coagulation in a number of patients. Our understanding of the problems of DIC was formulated on the grounds of a thirty-year study of the problem involving over 1,500 patients. Thereby, the conception of constant intravascular microcoagulation (CIMC) was developed with the following aims: to report the existing material and bring to researchers and doctors in practice information about the presence of the phenomenon of CIMC and to resolve debatable questions of definitions and practical usage of up-to-date information about DIC with the help of CIMC conception.

Disseminated Intravascular Coagulation: A Clinical/Laboratory Correlation In 48 Patients

1981 ◽  
Author(s):  
R L Bick
Keyword(s):  
Platelet Count ◽  
Disseminated Intravascular Coagulation ◽  
Clinical Laboratory ◽  
Fibrinogen Level ◽  
Degradation Products ◽  
Severe Bleeding ◽  
Thrombin Time ◽  
Intravascular Coagulation ◽  
At Iii ◽  
Pre Treatment

Disseminated intravascular coagulation (DIC) is a frequent clinical entity spanning from a moderately severe bleeding disorder to a catastrophic, fulminant, and often fatal form usually associated with hemorrhage or, less commonly,as diffuse thromboses. The clinical and laboratory features of DIC remain confusing and controversial. To critically evaluate the usefulness of coagulation tests in aiding in the diagnosis and monitoring of therapy in DIC the clinical and laboratory findings were summarized in 48 patients with DIC. All patients were subjected to a prothrombin time (PT), activated partial thromboplastin time (PTT), reptilase time (RT), thrombin time (TT), fibrin(ogen) degradation products (FDP), platelet count, protamine sulfate test (PSO4), fibrinogen determination, and biological antithrombin-III (AT-III) level at the time of diagnosis. In addition, these same laboratory modalities were used to monitor patients during and after therapy. In this series of 48 patients, 38 patients had acute DIC and 10 patients had chronic DIC. In those patients with acute DIC, 100% of patients presented with hemorrhage and 53% of patients had thrombosis; 26% of patients died of their DIC type syndrome. In those patients with chronic DIC, 100% presented with hemorrhage, 80% presented with thrombosis, and none died of their intravascular clotting process. The probability of a pre-treatment abnormality in acute DIC was: FDP > AT-III = platelet count PS04 > TT > PT > fibrinogen level > PTT > RT. The probability of pre-treatment abnormalties in chronic DIC was: FDP > PSO4 = PT > AT-III = RT platelet count fibrinogen level = TT. These studies suggest the FDP level, the AT-III level, PSO4, and fibrinogen level to be reliable for aiding in the diagnosis of acute DIC. In chronic DIC the fibrinogen level, PS04, PTT, and AT-III level appear to be the most reliable indicies.

Acute Viral Hepatitis with Epidemiological Focus on Hepatitis A Virus Infection and Its Clinical Course in Adults

2019 ◽  
Vol 4 (10) ◽  
Author(s):  
Manjushree Nayak ◽  
Jayanta Kumar Panda ◽  
Umesh Chandra Patra
Keyword(s):  
Liver Disease ◽  
Viral Infection ◽  
Hepatitis A ◽  
Acute Viral Hepatitis ◽  
Hepatitis A Virus ◽  
Clinical Course ◽  
Biochemical Profile ◽  
Severe Liver ◽  
Number Of Patients ◽  
Severe Liver Disease

In this prospective study, two hundred and fifty four patients diagnosed to be having AVH were analyzed with reference to clinical profile & viral markers and statistical analysis was done. Isolated viral infection was documented in 102 (40.1%) patients where as more than one hepatotrophic viruses caused AVH in 27(10.6%) patients. Non A-E Virus was the major case of sporadic AVH (40.1%), HBV & HEV were the etiological agent in 23.6% & 25.1% respectively. HAV was detected in 16.5% of the patients and the HCV was incriminated rarely as cause of sporadic AVH. The demographic, clinical and biochemical profile amongst isolated & mixed viral infection were found to be similar. However, HBV-AVH had significant prolonged course (p<0.001) and HAV-AVH was found to have significantly higher number of patients pursing a course of relapsing hepatitis. However HAV infection amongst adults in the present study was not found to cause severe liver disease except in few cases.

scholarly journals A Proposal of the Modification of Japanese Society on Thrombosis and Hemostasis (JSTH) Disseminated Intravascular Coagulation (DIC) Diagnostic Criteria for Sepsis-Associated DIC

2017 ◽  
Vol 24 (3) ◽  
pp. 439-445 ◽  
Author(s):  
Toshiaki Iba ◽  
Marcello Di Nisio ◽  
Jecko Thachil ◽  
Hideo Wada ◽  
Hidesaku Asakura ◽  
...  
Keyword(s):  
Critical Care ◽  
Platelet Count ◽  
Diagnostic Criteria ◽  
Disseminated Intravascular Coagulation ◽  
Japanese Society ◽  
Intravascular Coagulation ◽  
Risk Of Death ◽  
Antithrombin Activity ◽  
Number Of Patients ◽  
Multicenter Survey

Sepsis-associated disseminated intravascular coagulation (DIC) carries a high risk of death. Thus, a simple tool to quickly establish DIC diagnosis is required. The purpose of this study was to introduce the simple and reliable tool for the prediction of outcome in patients with sepsis complicated by coagulopathy. We investigated the performance of simplified Japanese Society on Thrombosis and Hemostasis (JSTH) DIC diagnostic criteria. In this study, we conducted a retrospective, multicenter survey in 107 general emergency and critical care centers in secondary and tertiary care hospitals. A total of 918 patients with sepsis-associated coagulopathy who underwent antithrombin supplementation were examined. The relationships between patient mortality and each of the baseline (ie, before treatment) JSTH-DIC diagnostic criteria were examined. A reduced platelet count, increased prothrombin time (PT) ratio, and lower antithrombin activity were correlated with 28-day mortality, while fibrinogen and fibrin degradation product (FDP) level were not. Thus, the number of points assigned to FDP levels was reduced from 3 to 1 (above 20 μg/mL). The simplified JSTH diagnostic criteria combining platelet count, PT ratio, antithrombin activity, and FDP level (reduction in the maximum score) strongly predicted 28-day mortality and allowed us to diagnose a larger/similar number of patients with DIC as compared to the original JSTH-DIC. The simplified JSTH-DIC diagnostic criteria show a similar performance to JSTH-DIC criteria in patients with septic coagulopathy. The lower number of laboratory markers used in the simplified JSTH-DIC score may increase its applicability and routine use in emergency and critical care setting.

Molecular Subunits and Transamidase Activity of Factor XIII During Disseminated Intravascular Coagulation in Acute Leukaemia

1980 ◽  
Vol 43 (01) ◽  
pp. 006-009 ◽  
Author(s):  
F Rodeghiero ◽  
T Barbui ◽  
R Battista ◽  
T Chisesi ◽  
G Rigoni ◽  
...  
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Acute Leukaemia ◽  
Factor Xiii ◽  
Thrombin Generation ◽  
Biologically Active ◽  
Thrombin Time ◽  
Transfusion Therapy ◽  
Subunit A ◽  
Intravascular Coagulation

SummaryThe "in vivo" thrombin generation which occurs during disseminated intravascular coagulation (DIC) leads to complex coagulation abnormalities. The subunit A of fibrin stabilizing factor (Factor XIII) is a sensitive target for thrombin whilst the subunit S, is not. The two subunits seem to be insensitive to plasmin.A typical DIC picture has been found in 15 out of 200 cases of acute leukaemia; the subunits and the transamidase activity (TA) of the enzyme were severely reduced. The biologically active component, subunit A, and its TA were found to be much more reduced (P < 0.001) in patients with DIC than in those with AML without typical laboratory DIC pattern ("controls"). The levels of subunit A were correlated only with fibrinogenaemia. No difference in subunit S levels was found between normal healthy subjects and "controls". On the other hand this subunit was significantly reduced in DIC patients.It is assumed that thrombin affects the zymogen Factor XIII leading to the activation product A2S which could be cleared from the circulation. An alternative explanation of the decrease of subunit S, insensitive to thrombin, could be sought in a defect of its synthesis which seems to be related to that of subunit A, as it has been shown in congenital Factor XIII deficiency.Haemorrhagic complications are common and often fatal in patients with acute leukaemia. Platelet transfusion therapy has reduced the risk of haemorrhage but there are cases, not responsive to platelets, in whom the haemostatic mechanism is altered, generally by disseminated intravascular coagulation (DIC) (1). This syndrome results from an exaggerated response to cell damage with release of thromboplastic substances which activate "in vivo" the coagulation system. Thus, the "in vivo" thrombin generation leads to a consumption pattern including reduced levels of platelets, fibrinogen, factor V, VIII and XIII; positive paracoagulation tests; prolonged thrombin time and increased fibrin degradation products (FDP). However, patients with haemorrhages, presumably due to DIC, do not always show all of the above laboratory features (2, 3). Moreover, conclusive and extensive clinical studies of the biological expression of the syndrome are missing especially in acute leukaemia. Consequently, the diagnostic criteria for DIC are not yet well established and the diagnostic or prognostic role of a single coagulation factor is not definitively known. Concerning Factor XIII in acute

scholarly journals The Treatment Intensity of Anticoagulant Therapy for Patients With Sepsis-Induced Disseminated Intravascular Coagulation and Outcomes: A Multicenter Cohort Study

2019 ◽  
Vol 25 ◽  
pp. 107602961983915
Author(s):  
Daisuke Kudo ◽  
Mineji Hayakawa ◽  
Hiroaki Iijima ◽  
Kazuma Yamakawa ◽  
Shinjiro Saito ◽  
...  
Keyword(s):  
Cohort Study ◽  
Hospital Mortality ◽  
Anticoagulant Therapy ◽  
Disseminated Intravascular Coagulation ◽  
High Intensity ◽  
Anticoagulation Therapy ◽  
Multicenter Cohort Study ◽  
Intravascular Coagulation ◽  
Low Intensity ◽  
Number Of Patients

We examined the institutional variations in anticoagulation therapy for sepsis-induced disseminated intravascular coagulation (DIC) and their effects on patient outcomes. This post hoc analysis of a cohort study included 3195 patients with severe sepsis across 42 intensive care units. To evaluate differences in the intensity of anticoagulation therapy, the proportion of patients receiving anticoagulation therapy and the total number of patients with sepsis-induced DIC were compared. Predicted in-hospital mortality for each patient was calculated using logistic regression analysis. To evaluate survival outcomes, the actual/mean predicted in-hospital mortality ratio in each institution was calculated. Thirty-eight institutions with 2897 patients were included. Twenty-five institutions treated 60% to 100% (high-intensity institutions), while the rest treated 0% to 50% (low-intensity institutions) of patients with sepsis-induced DIC having anticoagulant therapy. Every 10-unit increase in the intensity of anticoagulant therapy was associated with lower in-hospital mortality (odds ratio: 0.904). A higher number of high-intensity institutions (compared to low-intensity institutions) had lower in-hospital mortality and fewer bleeding events than predicted. In conclusion, institutional variations existed in the use of anticoagulation therapy in patients with sepsis-induced DIC. High-intensity anticoagulation therapy was associated with better outcomes.

Concentration of D-dimers in healthy cats and sick cats with and without disseminated intravascular coagulation (DIC)

2009 ◽  
Vol 11 (10) ◽  
pp. 842-846 ◽  
Author(s):  
Inger Tholen ◽  
Christiane Weingart ◽  
Barbara Kohn
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Underlying Disease ◽  
Latex Agglutination ◽  
Activated Partial Thromboplastin Time ◽  
Thrombin Time ◽  
Intravascular Coagulation ◽  
Specificity And Sensitivity ◽  
Healthy Control ◽  
Comparison Of The Results ◽  
D Dimer

The objective of this prospective study was to measure concentrations of D-dimers in 48 cats with various diseases and in 20 healthy cats to evaluate the sensitivity and specificity for D-dimers to diagnose disseminated intravascular coagulation (DIC). The cats were classified as having DIC if an underlying disease and at least three of the following criteria were present: thrombocytopenia, prolonged activated partial thromboplastin time, prothrombin time or thrombin time, schistocytes and/or a reduced antithrombin activity. D-dimer concentrations were measured using a semi-quantitative latex agglutination (LA) test (Accuclot D-Dimer, Sigma Diagnostics). The D-dimer test was positive for 8/12 cats with DIC and for 16/36 sick cats without DIC. D-dimers were negative for all healthy control cats. The comparison of the sick cats with DIC and those without DIC revealed a specificity and sensitivity of the D-dimer test of 56% and 67%; a comparison of the results for healthy cats and cats with DIC revealed a specificity and sensitivity of 100% and 67%, respectively. The D-dimer LA test is only of limited value for the diagnosis of DIC in cats.

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