On the Rôle of Disseminated Intravascular Coagulation in the Pathology of Birth Asphyxia

2008 ◽  
Vol 16 (5) ◽  
pp. 581-591 ◽  
Author(s):  
J. M. Anderson ◽  
J. K. Brown ◽  
F. Cockburn
Author(s):  
A. Kulikov

Presented material reveals main links in the pathogenesis of hemostatic disorder. In particular, attention is paid to the role of the lungs, liver and other organs in the development of this process. Role of vascular wall and blood cells in regulation of the physical state of blood is described in detail. The most frequent factors leading to hypercoagulation are indicated. Difference between hypercoagulation and thrombophilia is shown. The latter is found in clinical practice quite often, but at the same time, it is poorly diagnosed. Such a terrible complication of hemostatic disorder as disseminated intravascular coagulation is described. Its classification, stages of development, clinical manifestations are offered to the readers.


1994 ◽  
Vol 1 ◽  
pp. 210
Author(s):  
K. Okajima ◽  
M. Uchida ◽  
K. Murakami ◽  
H. Okabe ◽  
K. Takatsuki

1992 ◽  
Vol 41 (2) ◽  
pp. 71-75 ◽  
Author(s):  
H. Asakura ◽  
H. Jokaji ◽  
M. Saito C. Uotani ◽  
I. Kumabashiri ◽  
E. Morishita ◽  
...  

1999 ◽  
Vol 80 (5) ◽  
pp. 340-352
Author(s):  
F. B. Taylor Jr.

The experiences with primate models of E.coli sepsis with emphasis on the responses of the hemostatic system and the mechanism of these responses with emphasis on the role of phospholipid microparticles in mediating disseminated intravascular coagulation, (DIC) are discribed. Understanding the principles of how the hemostatic system responds to inflammatory stress depends on viewing this system as a collection of mediator and regulator factors. They are integrated into a balanced system consisting of four functional quadrants. Depending on circumstances this system is designed to control either the patency or the integrity of the cardiovascular system.


Blood ◽  
1980 ◽  
Vol 56 (1) ◽  
pp. 88-92 ◽  
Author(s):  
PB Neame ◽  
JG Kelton ◽  
IR Walker ◽  
IO Stewart ◽  
HL Nossel ◽  
...  

Abstract The mechanism of isolated thrombocytopenia in septicemia is unknown, but compensated disseminated intravascular coagulation (DIC) has been suggested as a possible cause. To investigate this possibility, platelet counts and sensitive assays for in vivo thrombin and plasmin generation, including fibrinogen gel chromatography and fibrinopeptide A (FPA) assays, were obtained on 31 septicemic patients. Fifteen of 17 patients with gram-negative septicemia and 8 of 14 patients with gram- positive septicemia had thrombocytopenia. Platelet survival studied demonstrated a decreased platelet survival. In 11 of 12 patients with severe thrombocytopenia (platelet count less than 50,000mul), there was laboratory evidence of intravascular coagulation. In contrast, there was little evidence of intravascular coagulation in 8 of 11 patients with moderate thrombocytopenia (platelet counts 50,000 to less than 150,000/mul) or in 7 of 8 patients with normal platelet counts. This report indicates that while DIC accompanies thrombocytopenia in many patients with severe thrombocytopenia, there is frequently little evidence for intravascular coagulation in patients with moderate thrombocytopenia. It is apparent that factors other than intravascular thrombin must play a role in producing the thrombocytopenia of septicemia.


2019 ◽  
Vol 178 ◽  
pp. 182-188 ◽  
Author(s):  
Satoshi Gando ◽  
Atsushi Shiraishi ◽  
Kazuma Yamakawa ◽  
Hiroshi Ogura ◽  
Daizoh Saitoh ◽  
...  

1998 ◽  
Vol 79 (06) ◽  
pp. 1111-1115 ◽  
Author(s):  
Satoshi Nanzaki ◽  
Shigeyuki Sasaki ◽  
Osamu Kemmotsu ◽  
Satoshi Gando

SummaryTo determine the role of plasma tissue factor on disseminated intravascular coagulation (DIC) in trauma and septic patients, and also to investigate the relationships between tissue factor and various thrombin markers, we made a prospective cohort study. Forty trauma patients and 20 patients with sepsis were classified into subgroups according to the complication of DIC. Plasma tissue factor antigen concentration (tissue factor), prothrombin fragment F1+2 (PF1+2), thrombin antithrombin complex (TAT), fibrinopeptide A (FPA), and D-dimer were measured on the day of admission (day 0), and on days 1, 2, 3, and 4 after admission. The levels of plasma tissue factor in the DIC group were more elevated than those of the non-DIC group in both the trauma and the septic patients. In patients with sepsis, tissue factor levels on days 0 through 4 in the non-DIC group showed markedly higher values than those in the control patients (135 ± 8 pg/ml). Significant correlations between tissue factor and PF1+2, TAT, FPA, and D-dimer were observed in the DIC patients, however, no such correlations were found in the non-DIC patients. These results suggest that elevated plasma tissue factor in patients with trauma and sepsis gives rise to thrombin generation, followed by intravascular coagulation.


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