Disseminated Intravascular Coagulation: An Update on Pathogenesis, Diagnosis, and Therapeutic Strategies.
Papageorgiou Chrysoula,Jourdi Georges,Adjambri Eusebe,Walborn Amanda,Patel Priya,Fareed Jawed,Elalamy Ismail,Hoppensteadt Debra,Gerotziafas Grigoris T
Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
Disseminated intravascular coagulation (DIC) is an acquired clinicobiological syndrome characterized by widespread activation of coagulation leading to fibrin deposition in the vasculature, organ dysfunction, consumption of clotting factors and platelets, and life-threatening hemorrhage. Disseminated intravascular coagulation is provoked by several underlying disorders (sepsis, cancer, trauma, and pregnancy complicated with eclampsia or other calamities). Treatment of the underlying disease and elimination of the trigger mechanism are the cornerstone therapeutic approaches. Therapeutic strategies specific for DIC aim to control activation of blood coagulation and bleeding risk. The clinical trials using DIC as entry criterion are limited. Large randomized, phase III clinical trials have investigated the efficacy of antithrombin (AT), activated protein C (APC), tissue factor pathway inhibitor (TFPI), and thrombomodulin (TM) in patients with sepsis, but the diagnosis of DIC was not part of the inclusion criteria. Treatment with APC reduced 28-day mortality of patients with severe sepsis, including patients retrospectively assigned to a subgroup with sepsis-associated DIC. Treatment with APC did not have any positive effects in other patient groups. The APC treatment increased the bleeding risk in patients with sepsis, which led to the withdrawal of this drug from the market. Treatment with AT failed to reduce 28-day mortality in patients with severe sepsis, but a retrospective subgroup analysis suggested possible efficacy in patients with DIC. Clinical studies with recombinant TFPI or TM have been carried out showing promising results. The efficacy and safety of other anticoagulants (ie, unfractionated heparin, low-molecular-weight heparin) or transfusion of platelet concentrates or clotting factor concentrates have not been objectively assessed.
Disseminated Intravascular Coagulation.
Seminars in oncology nursing
OBJECTIVES:This article describes the pathophysiology and causes of disseminated intravascular coagulation (DIC). Implications for nurses are also reviewed. DATA SOURCES:Pee-reviewed articles and up-to-date references were used to check accuracy of the information and provide information for current management of this syndrome. CONCLUSION:DIC is an oncologic emergency in which bleeding and clotting occur simultaneously. In the cancer population, the syndrome is frequently associated with certain malignancies or sepsis. If not recognized and treated early, mortality can be high. This article describes the risk factors that contribute to DIC, clinical manifestations of DIC, and its treatment. IMPLICATIONS FOR NURSING PRACTICE:Nurses need to consider the presenting diagnosis of the patient and understand laboratory abnormalities that signify DIC. The nurse plays a key role in early recognition of this syndrome as prompt treatment can reduce fatality.
Influence of high-dose antithrombin on platelet function and blood coagulation.
Miike Toru,Sakamoto Yuichiro,Narumi Shougo,Yoshitake Kunimasa,Sakurai Ryota,Nakayama Kento,Inoue Satoshi
Acute medicine & surgery
Aim:In healthy adults, there are sufficient amounts of antithrombin in the blood to regulate thrombin. However, the effects of high concentrations of antithrombin on dose-dependent anticoagulation and platelet function have not been reported. In this study, we assessed platelet function and blood coagulation following high-dose antithrombin supplementation . Methods:Blood samples were collected from 10 healthy volunteers, and samples with different antithrombin concentrations were prepared by adding an antithrombin agent (Neuart). Blood coagulation was assessed by the Thrombus-Formation Analysis System (T-TAS) and Rotational Thromboelastometry (ROTEM) using whole blood samples. Results:The data obtained by the platelet chip, exclusively representing platelet function, revealed that the onset of thrombus formation was significantly delayed in a dose-dependent manner (100%-200%, = 0.021; 100%-500%, = 0.011; 200%-500%, = 0.047). In measurements using the atheroma chip, which enables assessment of blood coagulation, the thrombus formation ability was found to be reduced (100%-200%, = 0.022; 100%-500%, = 0.05). In the ROTEM measurements, clotting time was prolonged in a dose-dependent manner (100%-200%: = 0.203, 200%-500%: = 0.005, 500%-1000%: = 0.022), except when comparing with 100% and 200%. Although antithrombin is reportedly saturated in healthy blood, its anticoagulant ability appears to be enhanced depending on its concentration. Furthermore, data obtained from the platelet chip showed that antithrombin might reduce platelet function. Conclusions:Antithrombin suppressed platelet function and blood coagulation in a dose-dependent manner.
Angiotensin Receptor Blockers Are Not Just for Hypertension Anymore.
Saavedra Juan M
Physiology (Bethesda, Md.)
Beyond blood pressure control, angiotensin receptor blockers reduce common injury mechanisms, decreasing excessive inflammation and protecting endothelial and mitochondrial function, insulin sensitivity, the coagulation cascade, immune responses, cerebrovascular flow, and cognition, properties useful to treat inflammatory, age-related, neurodegenerative, and metabolic disorders of many organs including brain and lung.