TREAT the underlying disorder! It is imperative that you fully evaluate the patient to determine the underlying cause and treat it appropriately. Don’t be afraid to load the boat as this is a sick patient and contact the MICU as this patient will need intensive care.
Therapies such as transfusions would temporize but not stop DIC. The strategy is to replace what is being consumed or lost.
Treat the underlying disease. For most cases, DIC will resolve on its own if the underlying condition is appropriately treated.
When possible, try to avoid the use of blood products to “fix labs” in a patient with asymptomatic DIC (although this may be warranted for profoundly low platelet count or fibrinogen level).
Sepsis-associated DIC generally causes patients to be prothrombotic. Therefore, holding DVT prophylaxis for patients with mild-moderate thrombocytopenia (e.g., platelet count >30,000) may be inadvisable.
As DIC can increase the risk of both thrombosis as well as bleeding, use of blood products is controversial. There is a lack of evidence on when to use these, so treatment is largely based on consensus opinion.
Trauma patients die from massive bleeding due to disseminated intravascular coagulation (DIC) with
a fbrinolytic phenotype in the early phase, which transforms to DIC with a thrombotic phenotype in
the late phase of trauma, contributing to the development of multiple organ dysfunction syndrome.
Disseminated intravascular coagulation (DIC) is a serious syndrome characterized by the systemic activation of blood coagulation resulting in the thrombosis of vessels leading to organ dysfunction and severe bleeding. When physicians try to treat DIC, it is imperative to diagnose and treat the underlying conditions. Anyone can be affected by DIC, but vulnerable groups such as pediatric populations, pregnant women and the elderly may be at higher risk.
Consider the following in the differential diagnosis of DIC: Vitamin K deficiency (normal platelet count), hemolytic uremic syndrome (coagulation assays within normal limits), thrombotic thrombocytopenic purpura (low ADAMTS13 activity), HELLP syndrome (hemolysis, elevated liver function tests, and low platelets).
Although the understanding of DIC and its underlying pathogenetic pathways has increased in recent decades, some important questions regarding the proper management of this coagulopathy remain. Current therapeutic interventions are mostly supportive and only partly effective, at best resulting in an amelioration of the derangement of coagulation or more rapid resolution of DIC; however, they have not been proven to result in an improvement of clinically relevant outcomes, such as organ failure or mortality.
An out of control coagulation and fibrinolytic cascade...
May be acute or chronic: Acute DIC has more bleeding, and chronic DIC has more thrombosis. PCC or other factor replacement is not helpful in treatment because it causes more thrombus formation, “fueling the fire”.
A half century ago, the concept of disseminated intravascular coagulation (DIC) was ridiculed to be an abbreviation for Disseminated International Confusion, because intravascular fibrin thrombosis was hardly ever found at autopsy. Since the end of last century, however, it has been emphasized that DIC equals a sign that “Death Is Coming”. DIC is now recognized an independent disease entity characterized by the intravascular activation of coagulation with loss of localization arising from different causes...
Disseminated intravascular coagulation (DIC) is an acquired syndrome of intravascular coagulation and is commonly encountered in critically ill patients. Think about DIC in the critically ill patient with oozing at vascular sites (or wounds)...
Treatment is directed at the underlying cause. Blood products may be indicated when active bleeding is present, or anticoagulation when thrombotic complications develop. Tranexamic acid is only used in DIC thought to be caused by an acute hyperfibrinolytic response such as trauma or obstetric-related DIC, but should be given within three hours of the insult. TXA is not recommended in other forms of DIC..
MANAGEMENT •treat cause! •FFP for APTT and INR •cryoprecipitate for fibrinogen (>1.0) •platelets for thrombocytopaenia (aim > 50) •consider FIIa •consider heparin if not bleeding (in chronic DIC).
The treatment of DIC involves two stages: treatment of the underlying disorder, which stops the triggering process, and supportive treatment to restore normal coagulation.
Transfusion protocols for DIC are complicated but in general should be based on whether there is clinical evidence of bleeding or need for an invasive procedure, rather than any specific ‘trigger’ value from laboratory tests.1 It is important to get urgent senior support and input from a haematologist.
Widespread and inappropriate activation of the coagulation and fibrinolytic systems. Either bleeding (65%) or thrombosis predominates. This can be caused by a variety of reasons...
DIC is a complex and highly variable disorder, whose manifestations depend upon the inciting event, the host response and underlying comorbid disease. Additionally, the morbidity and mortality in patients with DIC often depends more on the underlying disease and the specific pathophysiology.