Prevention of severe bleeding by tranexamic acid in a patient with disseminated intravascular coagulation

1990 ◽  
Vol 58 (2) ◽  
pp. 101-108 ◽  
Author(s):  
A. Takada ◽  
Y. Takada ◽  
T. Mori ◽  
S. Sakaguchi
Keyword(s):  
Tranexamic Acid ◽  
Disseminated Intravascular Coagulation ◽  
Severe Bleeding ◽  
Intravascular Coagulation

scholarly journals Successful treatment of an adult with Kasabach-Merritt syndrome using thalidomide, vincristine, and prednisone

2019 ◽  
Vol 47 (4) ◽  
pp. 1810-1814
Author(s):  
Yue-Hua Huang ◽  
Dao-Bin Zhou ◽  
Bing Han ◽  
Tian Li ◽  
Shu-Jie Wang
Keyword(s):  
Treatment Regimen ◽  
Disseminated Intravascular Coagulation ◽  
Tumor Regression ◽  
Severe Bleeding ◽  
Intravascular Coagulation ◽  
Subcutaneous Mass ◽  
Low Incidence ◽  
Disease Free ◽  
Novel Therapeutic

Objective Kasabach-Merritt syndrome is a rare disease that mainly occurs in infants and adolescents. It usually manifests as disseminated intravascular coagulation and severe bleeding, and is associated with high mortality. However, its low incidence and clinical rarity in adults mean that there is currently no well-verified treatment regimen for this disease. We report on an effective novel therapeutic regimen in a patient with Kasabach-Merritt syndrome. Methods A woman with Kasabach-Merritt syndrome presented with a recurrent subcutaneous mass and disseminated intravascular coagulation, and was treated with prednisone, vincristine and thalidomide. Results This treatment regimen successfully resolved the patient’s symptoms, with tumor regression. The patient remained disease-free after 6 years of follow-up. Conclusions Prednisone combined with vincristine and thalidomide may be an effective treatment for Kasabach-Merritt syndrome, but further studies are needed to verify the use of this regimen.

Case 17: Severe bleeding complications, lymphocytosis and leukoerythroblastosis – disseminated intravascular coagulation in a patient with metastasizing carcinoma of the prostate and chronic lymphocytic leukemia

1999 ◽  
Vol 56 (9) ◽  
pp. 533-536 ◽  
Author(s):  
Solenthaler ◽  
Lämmle
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Disseminated Intravascular Coagulation ◽  
Lymphocytic Leukemia ◽  
Bleeding Complications ◽  
Severe Bleeding ◽  
Disseminierte Intravasale Gerinnung ◽  
Intravascular Coagulation ◽  
Carcinoma Of The Prostate

Blutungskomplikationen bei chronischer lymphatischer Leukämie (CLL) stehen meist in Zusammenhang mit einer Thrombozytopenie, bedingt entweder durch eine direkte Verdrängung der Megakaryopoese bei diffuser Knochenmarksinfiltration oder durch einen vermehrten peripheren Verbrauch im Rahmen einer (sekundären) Immunthrombozytopenie. Eine disseminierte intravasale Gerinnung (DIC) gehört nicht zum Spektrum hämatologischer Komplikationen einer CLL. Das hier geschilderte Fallbeispiel eines Patienten mit schweren Blutungskomplikationen, labormäßigen Zeichen einer DIC und neu entdeckter CLL ließ eine Ursache der DIC vermissen. Das leukoerythroblastäre Blutbild lieferte den Schlüssel zur Diagnose eines metastasierenden Prostatakarzinoms, welches durch die Knochenmarksbiopsie bestätigt wurde und als Trigger für die DIC verantwortlich war.

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.

Disseminated Intravascular Coagulation With Trauma: Treatment With Exchange Transfusion

PEDIATRICS ◽  
1979 ◽  
Vol 63 (2) ◽  
pp. 337-339
Author(s):  
Ashok P. Sarnaik ◽  
Kenneth D. Stringer ◽  
Patrick F. Jewell ◽  
Sharada A. Sarnaik ◽  
Y. Ravindranath
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Exchange Transfusion ◽  
Hypovolemic Shock ◽  
Volume Overload ◽  
Trauma Treatment ◽  
Severe Bleeding ◽  
Clotting Factors ◽  
Traumatic Injuries ◽  
Intravascular Coagulation ◽  
History Of

Disseminated intravascular coagulation (DIC) may complicate hypovolemic shock secondary to trauma.1 Treatment with heparin in such cases is contraindicated because of the risk of bleeding at the site of trauma. Replacement therapy with clotting factors and platelets alone may be inadequate2 or result in volume overload in the presence of compromised renal function. We describe here a patient with multiple intraabdominal traumatic injuries whose severe bleeding diathesis secondary to DIC was successfully treated with exchange transfusion. CASE REPORT A 10-month-old black boy weighing 10 kg was brought to Children's Hospital of Michigan, Detroit with a history of grunting for three hours and "not feeling well" for three weeks.

Disseminated Intravascular Coagulation

1999 ◽  
Vol 82 (08) ◽  
pp. 695-705 ◽  
Author(s):  
Evert de Jonge ◽  
Tom van der Poll ◽  
Hugo ten Cate ◽  
Marcel Levi
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Clinical Management ◽  
Multiorgan Failure ◽  
Coagulation System ◽  
Clotting Factor ◽  
Bleeding Complications ◽  
Severe Bleeding ◽  
Search Term ◽  
Variable Intensity ◽  
Intravascular Coagulation

IntroductionA quick literature search in the MEDLINE databases from 1966 to 1998 using the search term disseminated intravascular coagulation (DIC) and related key words yields an impressive 11,921 manuscripts. Most of the published literature concerns the pathophysiology of DIC, which in its main features is now well understood. Other aspects of DIC, however, particularly those related to the definition, the relevance of the syndrome, and clinical management, remain unclear. Taking an evidence-based approach to the appropriate diagnosis and treatment of patients with DIC is difficult, in view of the lack of sound clinical trials. This is probably due to the fact that DIC is a poorly-defined syndrome with a widely variable intensity, often complicating a diversity of severe disorders that are themselves related to extensive morbidity and mortality.1,2 This chapter briefly reviews the clinical setting, incidence, and relevance of DIC and current insights into the pathogenesis of DIC. It also discusses the available knowledge on the clinical management of patients with this syndrome.DIC is not a disease or a symptom but rather a syndrome, which is always secondary to an underlying disorder. The syndrome is characterized by a systemic activation of the blood coagulation system, which results in the generation and deposition of fibrin, leading to microvascular thrombi in various organs and contributing to the development of multiorgan failure. Consumption and subsequent exhaustion of coagulation proteins and platelets, due to the ongoing activation of the coagulation system, may induce severe bleeding complications, although microclot formation may occur in the absence of severe clotting factor depletion and bleeding.3 Derangement of the fibrinolytic system further contributes to intravascular clot formation (discussed later), but in some cases accelerated fibrinolysis (e.g., due to consumption of α2-antiplasmin) may cause severe bleeding. Hence, a patient with DIC can present with simultaneous thrombotic and bleeding problems, which obviously complicates treatment. Although there is no general consensus regarding the definition of DIC, the definition as put forward by Müller-Berghaus and colleagues in 1995 might be most appropriate: “Disseminated intravascular coagulation is an acquired syndrome characterized by the activation of intravascular coagulation up to intravascular fibrin formation. The process may be accompanied by secondary fibrinolysis or inhibited fibrinolysis.”4

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