scholarly journals Prognostic value of prothrombin time and activated partial thromboplastin time in patients with posttraumatic disseminated intravascular coagulation.

1994 ◽  
Vol 5 (7) ◽  
pp. 723-724
Author(s):  
Satoshi Gando ◽  
Satoshi Nanzaki ◽  
Takashi Kameue ◽  
Hiroshi Makise ◽  
Yoshimi Nakanishi
Author(s):  
N. V. Galeeva ◽  
I. E. Kravchenko

Goal of the study is to reveal the particular features of hemostasis in patients with chronic hepatitis C in dynamics of natural course of disease. Materials and methods. The indices of hemostasis in 535 patients with chronic hepatitis C were assessed by the number of platelets, degree of their aggregation with the use of inductor of adenosine triphosphate and without it (spontaneous aggregation of platelets). Coagulative hemostasis was analyzed by the activated partial thromboplastin time, antitrombin III, prothrombin ratio, prothrombin time, fibrinogen concentration in plasma and international normalized ratio. Based on the number of Tr, typical for the disseminated intravascular coagulation syndrome, conditionally the patients were divided into 3 groups: I group - hypercoagulability; II - transient phase between hyper and hypocoagulation and III- hypocoagulation, which also included patients with liver cirrhosis. Results and discussion. Independent on the phase of disseminated intravascular coagulation syndrome, increase of aggregation of Tr with the growth of maximal amplitude was observed. The main part of studied indices of coagulative hemostasis indicated at the condition of hypocoagulation in patients with chronic hepatitis C - this is significant increase of activated partial thromboplastin time, prothrombin time, international normalized ratio and decrease of fibrinogen concentration in the studied groups by the phases of disseminated intravascular coagulation syndrome. Value of antitrombin III changed oppositely, it decreased, so that plasma hemostasis tends to the hypercoagulation. Conclusion. Under the chronic hepatitis C all phases of disseminated intravascular coagulation syndrome were observed with the disorder of thrombocytic coagulative hemostasis. There was followed up multidirectional change of hemostasis which obtained in the most cases character of delitescent course of disseminated intravascular coagulation syndrome.


Author(s):  
N. V. Galeeva ◽  
I. E. Kravchenko

Goal of the study is to reveal the particular features of hemostasis in patients with chronic hepatitis C in dynamics of natural course of disease. Materials and methods. The indices of hemostasis in 535 patients with chronic hepatitis C were assessed by the number of platelets, degree of their aggregation with the use of inductor of adenosine triphosphate and without it (spontaneous aggregation of platelets). Coagulative hemostasis was analyzed by the activated partial thromboplastin time, antitrombin III, prothrombin ratio, prothrombin time, fibrinogen concentration in plasma and international normalized ratio. Based on the number of Tr, typical for the disseminated intravascular coagulation syndrome, conditionally the patients were divided into 3 groups: I group - hypercoagulability; II - transient phase between hyper and hypocoagulation and III- hypocoagulation, which also included patients with liver cirrhosis. Results and discussion. Independent on the phase of disseminated intravascular coagulation syndrome, increase of aggregation of Tr with the growth of maximal amplitude was observed. The main part of studied indices of coagulative hemostasis indicated at the condition of hypocoagulation in patients with chronic hepatitis C - this is significant increase of activated partial thromboplastin time, prothrombin time, international normalized ratio and decrease of fibrinogen concentration in the studied groups by the phases of disseminated intravascular coagulation syndrome. Value of antitrombin III changed oppositely, it decreased, so that plasma hemostasis tends to the hypercoagulation. Conclusion. Under the chronic hepatitis C all phases of disseminated intravascular coagulation syndrome were observed with the disorder of thrombocytic coagulative hemostasis. There was followed up multidirectional change of hemostasis which obtained in the most cases character of delitescent course of disseminated intravascular coagulation syndrome.


2013 ◽  
Vol 58 (No. 11) ◽  
pp. 587-590 ◽  
Author(s):  
I. Uhrikova ◽  
K. Machackova ◽  
L. Rauserova-Lexmaulova ◽  
K. Rehakova ◽  
J. Doubek

Gastric dilatation and volvulus syndrome is associated with changes in haemostatic profiles. The aims of this study were to compare selected haemostatic and fibrinolytic parameters between healthy dogs and dogs with gastric dilatation and volvulus syndrome, estimate the incidence of disseminated intravascular coagulation (DIC), and determine the most sensitive test for detection of DIC in these patients. Blood was collected from 22 dogs with gastric dilatation and volvulus syndrome, and nine healthy control dogs. Platelet counts, prothrombin time, activated partial thromboplastin time, fibrinogen concentrations and fibrin/fibrinogen degradation products were measured in all control dogs and patients with gastric dilatation and volvulus syndrome, before and after surgery. Significant differences between control dogs and patients were seen in activated partial thromboplastin time and fibrin/fibrinogen degradation products before surgery and all measured parameters after surgery. The incidence of DIC was 59%. The most sensitive tests for detection of DIC before surgery were those for activated partial thromboplastin time and fibrin/fibrinogen degradation products.


Blood ◽  
1990 ◽  
Vol 76 (8) ◽  
pp. 1538-1545 ◽  
Author(s):  
KC Day ◽  
LC Hoffman ◽  
MO Palmier ◽  
KK Kretzmer ◽  
MD Huang ◽  
...  

Lipoprotein-associated coagulation inhibitor produces feed-back inhibition of tissue factor (tissue thromboplastin)-induced coagulation in the presence of factor Xa Recombinant lipoprotein-associated coagulation inhibitor (rLACI) was tested for its ability to modify thromboplastin-induced intravascular coagulation in a rabbit model that allows monitoring of iodine-125 fibrin accumulation/disappearance in the lung and sampling of blood for the measurement of coagulation parameters. Infusion of thromboplastin into the rabbit caused a rapid increase of radioactivity over the lungs, possibly due to the accumulation of 125I fibrin in the lungs, followed by a rapid decline of radioactivity, suggestive of removal of fibrin from the lungs. Thromboplastin also caused a rapid decrease of systemic fibrinogen that was accompanied by a lengthening of the activated partial thromboplastin time and prothrombin time. The effect of coinfusion of rLACI with thromboplastin or bolus injection of rLACI before thromboplastin infusion was studied. At a high dose of rLACI (800 micrograms/kg body weight), the thromboplastin-induced radioactivity increase in the lungs and the systemic fibrinogen decrease were completely suppressed. The activated partial thromboplastin time and prothrombin time of the plasma samples lengthened, possibly due to the presence of thromboplastin in circulation. The thromboplastin-induced radioactivity increase over the lungs was not completely suppressed by lower doses of rLACI (135 to 270 micrograms/kg body weight), but these doses of rLACI prevented systemic fibrinogen decrease. At a bolus dose of 23 micrograms/kg body weight, rLACI provided 50% protection of the fibrinogen consumption (fibrinogen decreased to 82% compared with 65% in rabbits treated with thromboplastin alone). These results show that rLACI is effective in the inhibition of thromboplastin-induced coagulation in vivo.


Blood ◽  
1976 ◽  
Vol 47 (2) ◽  
pp. 287-296 ◽  
Author(s):  
DH Wigton ◽  
GJ Kociba ◽  
EA Hoover

The objective of this study was to characterize the hemostatic defect in dogs with infectious canine hepatitis (ICH), a naturally occurring viral disease of dogs. Five littermate dogs were inoculated with 10(3) TCID50 of ICH virus intravenously. Two littermates were controls. The clinicopathologic manifestations of ICH were fever, depression, anorexia, hematemesis, melena, widespread mucocutaneous petechiae, prolonged bleeding from venipunctures, faceial edema, leukopenia, and proteinuria. The hemostatic defect of ICH was characterized by thrombocytopenia, abnormal platelet function, prolonged one-stage prothrombin time and activated partial thromboplastin time, normal thrombin times, depressed factor VIII activity, and increased fibrin- fibrinogen degradation products. These findings suggested that the central pathologic mechanism of the abnormal hemostasis in ICH was disseminated intravascular coagulation (DIC). ICH is an example of DIC induced by viral infection. This disease is a suitable model for investigation of the detection, pathogenesis, and therapy of DIC.


2000 ◽  
Vol 2 (2) ◽  
pp. 115-119 ◽  
Author(s):  
A E Ridyard ◽  
E A Welsh ◽  
D A Gunn-Moore

A peri-parturient fifteen-month-old female Maine Coon cat was presented with extreme weakness and depression, profound hypovolaemia and hypothermia. Severe hyperkalaemia, hyponatraemia and anaemia were detected. Disseminated intravascular coagulation was suspected due to marked prolongation of activated partial thromboplastin time. Uterine torsion was diagnosed at exploratory laparotomy. The cat made a full recovery following ovariohysterectomy and intensive supportive therapy.


Blood ◽  
1990 ◽  
Vol 76 (8) ◽  
pp. 1538-1545 ◽  
Author(s):  
KC Day ◽  
LC Hoffman ◽  
MO Palmier ◽  
KK Kretzmer ◽  
MD Huang ◽  
...  

Abstract Lipoprotein-associated coagulation inhibitor produces feed-back inhibition of tissue factor (tissue thromboplastin)-induced coagulation in the presence of factor Xa Recombinant lipoprotein-associated coagulation inhibitor (rLACI) was tested for its ability to modify thromboplastin-induced intravascular coagulation in a rabbit model that allows monitoring of iodine-125 fibrin accumulation/disappearance in the lung and sampling of blood for the measurement of coagulation parameters. Infusion of thromboplastin into the rabbit caused a rapid increase of radioactivity over the lungs, possibly due to the accumulation of 125I fibrin in the lungs, followed by a rapid decline of radioactivity, suggestive of removal of fibrin from the lungs. Thromboplastin also caused a rapid decrease of systemic fibrinogen that was accompanied by a lengthening of the activated partial thromboplastin time and prothrombin time. The effect of coinfusion of rLACI with thromboplastin or bolus injection of rLACI before thromboplastin infusion was studied. At a high dose of rLACI (800 micrograms/kg body weight), the thromboplastin-induced radioactivity increase in the lungs and the systemic fibrinogen decrease were completely suppressed. The activated partial thromboplastin time and prothrombin time of the plasma samples lengthened, possibly due to the presence of thromboplastin in circulation. The thromboplastin-induced radioactivity increase over the lungs was not completely suppressed by lower doses of rLACI (135 to 270 micrograms/kg body weight), but these doses of rLACI prevented systemic fibrinogen decrease. At a bolus dose of 23 micrograms/kg body weight, rLACI provided 50% protection of the fibrinogen consumption (fibrinogen decreased to 82% compared with 65% in rabbits treated with thromboplastin alone). These results show that rLACI is effective in the inhibition of thromboplastin-induced coagulation in vivo.


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