In the clinical settings, disseminated intravascular coagulation (DIC) and complications such as hemorrhage are commonly seen in acute promyelocytic leukemia patients, whereas thrombosis is rarely reported. We reported a case here that the patient presented with cerebral infarction as the first manifestation. During the admission, the patient encountered differentiation syndrome, pulmonary embolism, pulmonary hemorrhage, and myocardial ischemia, as well as bleeding and thrombosis complications. Hence the patient was diagnosed as DIC. After the treatment of blood transfusion instead of anticoagulation, his condition was stable and the remission was completely achieved. The treatment experience provides guides for other patients with similar complications of simultaneous bleeding and thrombosis.
Blood Coagulation ; Cerebral Infarction ; Disseminated Intravascular Coagulation ; etiology ; Humans ; Leukemia, Promyelocytic, Acute ; complications ; Thrombosis

OBJECTIVETo investigate the risk factors for early disseminated intravascular coagulation (DIC) in neonates with sepsis.

METHODSA retrospective clinical study was performed on 100 neonates with a confirmed diagnosis of sepsis between 2012 and 2013. The children were classified into normal coagulation group, non-overt DIC group (early DIC group), and overt DIC group (late DIC group) based on the ISTH overt DIC scoring system. The clinical manifestations and risk factors were analyzed statistically.

RESULTSEarly DIC occurred in 44 (44%) cases in the 100 neonates with sepsis. The incidence of sclerema showed significant differences between the three groups (P<0.05). Asphyxia, bleeding, and Gram-negative bacterial infection were independent risk factors for early DIC.

CONCLUSIONSCoagulation function should be actively monitored and early intervention measures should be taken for neonates with asphyxia, bleeding, and Gram-negative bacterial infection to prevent early DIC from progressing to late DIC.

Disseminated Intravascular Coagulation ; etiology ; Female ; Humans ; Infant, Newborn ; Logistic Models ; Male ; Risk Factors ; Sepsis ; complications

Transitional cell carcinoma has rarely been reported to be associated with disseminated intravascular coagulation (DIC). We report a 55-year-old Chinese man who was diagnosed with transitional cell carcinoma with vertebral metastasis. He presented with severe anaemia and thrombocytopenia, and subsequent evaluation revealed features of DIC. Interestingly, he did not have fever, any localising symptoms or signs of infection. He was treated aggressively with transfusion of packed cells, platelets, intravenous vitamin K and fresh frozen plasma. Despite aggressive treatment, the coagulation abnormalities were resistant to correction. The patient continued to deteriorate and eventually died of cardiac arrest. This case illustrates that transitional cell carcinoma can also be associated with DIC, possibly due to the expression of certain unidentified procoagulant factors similar to the tissue factor responsible for DIC.
Anemia ; etiology ; Carcinoma, Transitional Cell ; blood ; complications ; Disseminated Intravascular Coagulation ; etiology ; Humans ; Male ; Middle Aged ; Ureteral Neoplasms ; blood ; complications

Maternal septic shock and disseminated intravascular coagulation (DIC) following amniocentesis is a relatively rare condition, and its incidence is only 0.03~0.19%. Acute myocardial infarction (AMI) associated with DIC is also rare. We report here on a 40-year-old female patient who had septic shock and DIC that was complicated by AMI following amniocentesis. The possible mechanism of AMI in this patient may have been coronary artery thrombosis associated with DIC.
Shock, Septic/*etiology ; Pregnancy ; Myocardial Infarction/*etiology ; Humans ; Female ; Disseminated Intravascular Coagulation/*complications/*etiology ; Amniocentesis/*adverse effects ; Adult

Betacoronavirus ; COVID-19 ; Coronavirus Infections/complications* ; Disseminated Intravascular Coagulation/etiology* ; Humans ; Pandemics ; Pneumonia, Viral/complications* ; SARS-CoV-2

Betacoronavirus ; Blood Coagulation Disorders ; epidemiology ; etiology ; Coronavirus Infections ; complications ; Disseminated Intravascular Coagulation ; epidemiology ; etiology ; Fibrin Fibrinogen Degradation Products ; analysis ; Humans ; Pandemics ; Pneumonia, Viral ; complications ; Venous Thromboembolism ; epidemiology ; etiology

Acute coagulopathy of trauma-shock (ACoTS) occurs in 25% of patients with severe trauma in the early phase, and the mortality of those patients is four-fold higher than patients without coagulopathy. The pathophysiology of this complicated phenomenon has been focused on in recent years. Tissue injury and hypoperfusion, activated protein C and Complements play important roles in the early phase after trauma. While the use of blood products, hypothermia, acidosis and inflammation are the main mechanism in late phase. Supplementing coagulation factors and platelets to improve ACoTS are inefficient. Only positive resuscitation from shock and improving tissue hypoperfusion have expected benefits.
Blood Coagulation Disorders ; etiology ; Complement System Proteins ; physiology ; Disseminated Intravascular Coagulation ; etiology ; Humans ; Hypothermia ; complications ; Inflammation ; complications ; Protein C ; physiology ; Shock, Traumatic ; complications

Abruptio Placentae ; complications ; Adult ; Disseminated Intravascular Coagulation ; diagnosis ; etiology ; therapy ; Female ; Humans ; Infant, Newborn ; Male ; Pregnancy ; Prognosis ; Risk Factors

Anticoagulants ; therapeutic use ; Disseminated Intravascular Coagulation ; drug therapy ; etiology ; Heparin ; therapeutic use ; Humans ; Leukemia, Promyelocytic, Acute ; complications

Trauma-induced coagulopathy is classified into primary and secondary coagulopathy, with the former elicited by trauma and traumatic shock itself and the latter being acquired coagulopathy induced by anemia, hypothermia, acidosis, and dilution. Primary coagulopathy consists of disseminated intravascular coagulation and acute coagulopathy of trauma shock (ACOTS). The pathophysiology of ACOTS is the suppression of thrombin generation and neutralization of plasminogen activator inhibitor-1 mediated by activated protein C that leads to hypocoagulation and hyperfibrinolysis in the circulation. This review tried to clarify the validity of activated protein C hypothesis that constitutes the main pathophysiology of the ACOTS in experimental trauma models.
Acute Disease ; Animals ; Blood Coagulation Disorders ; etiology ; Disease Models, Animal ; Disseminated Intravascular Coagulation ; etiology ; Humans ; Mice ; Plasminogen Activator Inhibitor 1 ; Protein C ; physiology ; Thrombin ; Wounds and Injuries ; complications