Causes, Risk Factors, And Complications Of Disseminated Intravascular Coagulation (DIC)
Disseminated intravascular coagulation (DIC) causes the production of blood clots in an individual's small blood vessels that can obstruct blood flow to organs in the affected region. Clotting factors and platelets are components of the blood required for proper and effective blood clots formation. The former is a condition where the clotting factors become more active than usual, resulting in inappropriate blood clot formation. It can be acute and occur suddenly, or it may be chronic and develop slowly. This condition is diagnosed through a variety of tests. They include a physical exam, medical history, complete blood count, blood smear, serum fibrinogen, and fibrin degradation tests. Treatment is based on symptoms and may include blood transfusions, oxygen therapy, and other medications.
Disseminated intravascular coagulation treatment depends on the symptoms and underlying cause. However, prescription medications are quite common. Patients can receive anticoagulants, such as heparin, to clot their blood. Many acute cases are treated with hospitalization. Blood and plasma transfusions can help as well, and some patients will need oxygen therapy. Of course, patients must understand the causes and complications of disseminated intravascular coagulation first.
Infection Or Inflammation
An individual's infection or inflammation may cause disseminated intravascular coagulation. The most common bacterial infections implicated in this condition are gram-positive blood infections, rickettsia infections, and gram-negative blood infections. Some viral infections have also been involved in developing this condition, including human immunodeficiency virus, varicella-zoster virus, cytomegalovirus, and hepatitis viruses. Fungal Histoplasma infections and parasitic malaria infections have also been seen to induce disseminated intravascular coagulation. The systemic influx of proinflammatory cytokines results from microorganisms' specific cell membrane components. This includes endotoxins and lipopolysaccharides.
Large amounts of cytokines can stimulate the production and expression of a tissue factor that initiates the coagulation cascade. This results in inappropriate thrombin formation. Infections, such as pancreatitis, directly activate clotting factor X and elevate thrombin activity in the systemic circulation, causing the improper formation of clots. As they are a probable cause, individuals who contract such infections or have systemic inflammation are at an increased risk of developing disseminated intravascular coagulation.
Brain Or Crush Injuries
An individual who has experienced brain or crush injuries is at an increased risk of developing disseminated intravascular coagulation. This is due to the association between it and severe trauma. Brain injuries that occur due to trauma and crush injuries can induce this condition through a combination of different mechanisms. Crush injuries are known to cause a mass rupture of thousands of cells simultaneously upon bodily impact. This cause of cellular apoptosis induces the bulk release of tissue materials such as phospholipids and tissue factor into the patient's systemic circulation.
Crush injuries also cause a large volume of hemolysis (red blood cell destruction) on top of extensive damage to the blood vessel walls. Combining these mechanisms is thought to induce the coagulation cascade's reactive activation in multiple systems in the body. Individuals who suffer from brain or crush injuries involving trauma have almost identical sequencing of system-wide inflammatory cytokines as patients affected by a septic infection of the blood. It is difficult to pinpoint the exact processes of disseminated intravascular coagulation development in every brain and crush injury patient. However, the release of materials, extensive damage, and actions of a mass cytokine influx are thought to play critical roles.
