Intravascular Coagulation as a Clinical Manifestation of the Shwartzman Reaction

2015 ◽  
pp. 41-48
Author(s):  
Wataru Mori
Keyword(s):  
Clinical Manifestation ◽  
Intravascular Coagulation ◽  
Shwartzman Reaction

Consumption of Hageman Factor Activity in the Generalized Shwartzman Reaction Induced by Liquoid

1970 ◽  
Vol 23 (02) ◽  
pp. 386-404 ◽  
Author(s):  
G Müller-Berghaus ◽  
H. G Lasch
Keyword(s):  
Partial Thromboplastin Time ◽  
Lethal Dose ◽  
Control Group ◽  
Factor V ◽  
Consumption Coagulopathy ◽  
Factor Activity ◽  
Hageman Factor ◽  
Intravascular Coagulation ◽  
Shwartzman Reaction

SummaryThe role of Hageman factor in triggering intravascular coagulation has been studied in rabbits injected intravenously with Liquoid. Besides changes of coagulation parameters characteristic of consumption coagulopathy (e.g. decrease in platelet counts, fibrinogen levels, factor V activity), a pronounced drop in Hageman factor activity was observed after injection of Liquoid. Likewise, the partial thromboplastin time became prolonged.The activation of Hageman factor in vivo could be prevented by intravenous infusion of lysozyme. Twenty min after starting the lysozyme infusion, the partial thromboplastin time became prolonged from a mean of 29 sec to 108 sec. Animals infused with lysozyme and injected with a lethal dose of Liquoid did not develop a consumption coagulopathy. In the same manner, none of 10 animals treated with lysozyme developed the generalized Shwartzman reaction, whereas in the control group 19 out of 20 animals showed fibrin thrombi in the glomerular capillaries.From the present study it may be concluded that the intravascular coagulation process after intravenous injection of Liquoid is triggered by Hageman factor activation.

scholarly journals Immunodepletion of extrinsic pathway inhibitor sensitizes rabbits to endotoxin-induced intravascular coagulation and the generalized Shwartzman reaction

Blood ◽  
1991 ◽  
Vol 78 (6) ◽  
pp. 1496-1502 ◽  
Author(s):  
PM Sandset ◽  
BJ Warn-Cramer ◽  
SL Maki ◽  
SI Rapaport
Keyword(s):  
Factor Viia ◽  
Factor V ◽  
Activity Levels ◽  
Cell Surfaces ◽  
Extrinsic Pathway ◽  
Intravascular Coagulation ◽  
Disease States ◽  
Shwartzman Reaction ◽  
Thrombotic Complications

Abstract We have reported earlier that immunodepletion of extrinsic pathway inhibitor (EPI) sensitizes rabbits to disseminated intravascular coagulation (DIC) induced by infusing a low concentration of tissue factor (TF). We now describe the effect of immunodepletion of EPI in rabbits administered endotoxin. Cortisone-treated rabbits were administered anti-rabbit EPI immunoglobulin (IgG) or Fab fragments or were administered control nonimmune material before an injection of endotoxin. In four of seven rabbits administered anti-EPI, plasma EPI activity levels were reduced by 70% to 80% of initial levels for 6 to 8 hours. In these rabbits the endotoxin induced extensive DIC, as evidenced by substantial decreases in fibrinogen, factor V, factor VIII, and platelets, and gross hemorrhagic necrosis of the kidneys due to massive deposition of fibrin in the glomerular microcirculation (the generalized Shwartzman reaction). In three rabbits administered anti- EPI, plasma EPI levels were only transiently reduced. In these rabbits and in four rabbits administered nonimmune IgG or Fab, endotoxin induced minimal to moderate intravascular clotting and deposits of fibrin were not found in the glomerular capillaries. Because it is believed that TF expressed on monocytes triggers endotoxin-induced coagulation, these data are taken as evidence that EPI functions as a natural anticoagulant that can regulate factor VIIa/TF activity expressed on cell surfaces in vivo. They support a hypothesis that EPI prevents thrombotic complications that might otherwise result from exposure of blood to cytokine-induced generation of small amounts of TF on cell surfaces in many inflammatory and infectious disease states.

scholarly journals Editorial: Intravascular Coagulation, the Shwartzman Reaction and the Pathogenesis of T.T.P

Blood ◽  
1964 ◽  
Vol 24 (6) ◽  
pp. 775-779 ◽  
Author(s):  
ROBERT N. TAUB ◽  
F. RODRIGUEZ-ERDMANN ◽  
WILLIAM DAMESHEK
Keyword(s):  
Intravascular Coagulation ◽  
Shwartzman Reaction

scholarly journals THE PREVENTION OF THE GENERALIZED SHWARTZMAN REACTION WITH SODIUM WARFARIN

1958 ◽  
Vol 107 (3) ◽  
pp. 377-381 ◽  
Author(s):  
Sandor S. Shapiro ◽  
Donald G. McKay
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Control Group ◽  
Cortical Necrosis ◽  
Renal Cortical Necrosis ◽  
Intravascular Coagulation ◽  
Intravenous Injections ◽  
Bacterial Endotoxins ◽  
Shwartzman Reaction ◽  
Kidney Liver ◽  
Intravenous Sodium

Using intravenous sodium warfarin, rabbits were rendered hypoprothrombinemic and subjected to two intravenous injections of Shear's polysaccharide. None of the 9 animals surviving the required period of time developed bilateral renal cortical necrosis or histologic thrombi in the kidney, liver, spleen, or lungs. In a control group of 7 animals treated only with endotoxin, 6 developed bilateral renal cortical necrosis. It is concluded that the prothrombin complex is necessary for the production of the generalized Shwartzman reaction by bacterial endotoxins and that this phenomenon is essentially a process of disseminated intravascular coagulation.

Mycobacterium tuberculosis inducing disseminated intravascular coagulation

2005 ◽  
Vol 93 (04) ◽  
pp. 729-734 ◽  
Author(s):  
Jann-Yuan Wang ◽  
Po-Ren Hsueh ◽  
Yuang-Shuang Liaw ◽  
Wen-Yi Shau ◽  
Pan-Chyr Yang ◽  
...  
Keyword(s):  
Mortality Rate ◽  
Clinical Manifestation ◽  
Disseminated Intravascular Coagulation ◽  
Early Stage ◽  
Prognostic Significance ◽  
Clinical Manifestations ◽  
Clinical Findings ◽  
Mediastinal Lymphadenopathy ◽  
Disseminated Tuberculosis ◽  
Intravascular Coagulation

SummaryDisseminated 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.

scholarly journals Immunodepletion of extrinsic pathway inhibitor sensitizes rabbits to endotoxin-induced intravascular coagulation and the generalized Shwartzman reaction

Blood ◽  
1991 ◽  
Vol 78 (6) ◽  
pp. 1496-1502 ◽  
Author(s):  
PM Sandset ◽  
BJ Warn-Cramer ◽  
SL Maki ◽  
SI Rapaport
Keyword(s):  
Factor Viia ◽  
Factor V ◽  
Activity Levels ◽  
Cell Surfaces ◽  
Extrinsic Pathway ◽  
Intravascular Coagulation ◽  
Disease States ◽  
Shwartzman Reaction ◽  
Thrombotic Complications

We have reported earlier that immunodepletion of extrinsic pathway inhibitor (EPI) sensitizes rabbits to disseminated intravascular coagulation (DIC) induced by infusing a low concentration of tissue factor (TF). We now describe the effect of immunodepletion of EPI in rabbits administered endotoxin. Cortisone-treated rabbits were administered anti-rabbit EPI immunoglobulin (IgG) or Fab fragments or were administered control nonimmune material before an injection of endotoxin. In four of seven rabbits administered anti-EPI, plasma EPI activity levels were reduced by 70% to 80% of initial levels for 6 to 8 hours. In these rabbits the endotoxin induced extensive DIC, as evidenced by substantial decreases in fibrinogen, factor V, factor VIII, and platelets, and gross hemorrhagic necrosis of the kidneys due to massive deposition of fibrin in the glomerular microcirculation (the generalized Shwartzman reaction). In three rabbits administered anti- EPI, plasma EPI levels were only transiently reduced. In these rabbits and in four rabbits administered nonimmune IgG or Fab, endotoxin induced minimal to moderate intravascular clotting and deposits of fibrin were not found in the glomerular capillaries. Because it is believed that TF expressed on monocytes triggers endotoxin-induced coagulation, these data are taken as evidence that EPI functions as a natural anticoagulant that can regulate factor VIIa/TF activity expressed on cell surfaces in vivo. They support a hypothesis that EPI prevents thrombotic complications that might otherwise result from exposure of blood to cytokine-induced generation of small amounts of TF on cell surfaces in many inflammatory and infectious disease states.

scholarly journals RETICULOENDOTHELIAL CLEARANCE OF CIRCULATING FIBRIN IN THE PATHOGENESIS OF THE GENERALIZED SHWARTZMAN REACTION

1962 ◽  
Vol 115 (5) ◽  
pp. 1065-1082 ◽  
Author(s):  
Leung Lee
Keyword(s):  
Direct Consequence ◽  
Reticuloendothelial System ◽  
Protective Mechanism ◽  
Intravascular Coagulation ◽  
Intravenous Injections ◽  
Fibrin Formation ◽  
Shwartzman Reaction

Intravenous injections of endotoxin or infusions of thrombin in the rabbit initiate intravascular coagulation but do not usually result in massive deposition of fibrin. It has been proposed that the reticuloendothelial system may function efficiently in the removal of circulating fibrin; its blockade permits reproduction of all of the features of the generalized Shwartzman reaction by infusions of thrombin. In the rabbit the reticuloendothelial system may constitute the major protective mechanism against the vasculo-occlusive lesions of the generalized Shwartzman reaction, which appears to be the direct consequence of intravascular fibrin formation and deposition.

scholarly journals An Electron Microscopic Study of Thrombin-Induced Disseminated Intravascular Coagulation

Blood ◽  
1967 ◽  
Vol 29 (2) ◽  
pp. 169-181 ◽  
Author(s):  
WILLIAM MARGARETTEN ◽  
ILONA CSAVOSSY ◽  
DONALD G. McKAY
Keyword(s):  
Light Microscopy ◽  
Rat Kidney ◽  
Reticuloendothelial System ◽  
Electron Microscopic ◽  
Intravascular Coagulation ◽  
Major Mechanism ◽  
Shwartzman Reaction ◽  
Kidney Liver ◽  
Fibrin Thrombi ◽  
Glomerular Capillaries

Abstract Fibrin thrombi due to slow intravascular coagulation appear simultaneously in rat kidney, liver, lung, and spleen, although the kidney is the only organ to show fibrin by light microscopy. The strands of fibrin are frequently associated with aggregation and viscous metamorphosis of platelets, particularly in the lungs. Some fibrin is eliminated by the reticuloendothelial system and through damaged glomeruli, but the major mechanism of removal is intravascular dissolution. Ischemic changes secondary to thrombosis are more prominent in glomerular capillaries than in other tissues. The morphologic observations are discussed in relation to "preparation" for the generalized Shwartzman reaction.

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