Disseminated Intravascular Coagulation (DIC) is a serious, life-threatening medical condition. DIC is not a primary disease, but a complex disorder arising as a complication of an underlying illness or injury. It represents a widespread, abnormal activation of the body’s blood clotting system throughout the blood vessels. This activation can be rapid and severe, leading to a breakdown of the normal processes that keep blood flowing smoothly.
How DIC Disrupts the Body’s Clotting System
The mechanism of DIC involves the systemic activation of the coagulation cascade, the sequence of events that normally leads to blood clot formation. This process is initiated when blood contacts tissue factor, a protein not usually exposed to circulation. Once triggered, massive amounts of thrombin are generated, converting fibrinogen into insoluble fibrin strands.
These fibrin strands and aggregated platelets form countless small clots, or microthrombi, that deposit throughout the small blood vessels. This widespread microvascular clotting impedes normal blood flow and causes ischemia, leading to damage and potential failure in organs like the kidneys, lungs, and brain. This initial phase is characterized by excessive, uncontrolled clot formation.
The body attempts to manage this crisis by rapidly consuming its available clotting materials, including platelets and various coagulation factors. The natural clot-dissolving system, fibrinolysis, is also activated in response to the widespread fibrin deposition. This process breaks down the newly formed clots, releasing fibrin degradation products (FDPs), which include D-dimer.
The consumption of platelets and clotting factors, combined with FDPs that interfere with remaining clotting function, leads to a severe shortage of components for normal hemostasis. This state, known as consumption coagulopathy, shifts the balance from excessive clotting to severe, uncontrolled bleeding (hemorrhage). The dual nature of DIC—clotting followed by bleeding—arises because the body’s resources are exhausted controlling the initial widespread thrombosis.
Primary Underlying Causes and Risk Factors
DIC is always a complication of another medical problem and never occurs spontaneously. The underlying cause exposes the blood to procoagulant molecules, primarily tissue factor, which triggers the coagulation cascade. Sepsis, the body’s extreme response to infection, is the most common risk factor for developing DIC. Infections (bacterial, viral, fungal, or parasitic) lead to systemic inflammation that results in tissue factor release from endothelial cells and circulating leukocytes.
Major trauma, such as severe head injury, crush injuries, or extensive burns, commonly triggers DIC. Damage to large amounts of tissue releases significant quantities of tissue factor and other procoagulant materials into the bloodstream. Complications during pregnancy and childbirth are also well-known causes. Conditions like placental abruption or amniotic fluid embolism introduce thromboplastin-rich material into the mother’s circulation, initiating DIC.
Certain types of cancer, particularly acute promyelocytic leukemia and advanced solid tumors, are associated with chronic or acute DIC. Cancer cells can directly release tissue factor, leading to continuous, low-grade clotting activation. Less common triggers include severe immune reactions, such as incompatible blood transfusions or organ transplant rejection, and toxins like snake venom. Pancreatitis and liver disease can also contribute due to the release of enzymes or impaired clearance of clotting factors.
Recognizing the Signs and Medical Management
The physical signs of DIC reflect both the initial widespread clotting and the subsequent severe bleeding. Clotting symptoms manifest as organ dysfunction due to impaired blood flow. This can include confusion if the brain is affected, shortness of breath from lung damage, or decreased urine output indicating kidney injury. In severe cases, patients may develop cyanosis or gangrene in their fingers and toes (acral cyanosis) due to blocked small blood vessels.
Signs of the later bleeding phase are often more noticeable, including persistent oozing from IV sites or surgical wounds. Patients may exhibit petechiae (tiny red or purple spots) or larger patches of bruising called ecchymoses. Internal bleeding can also occur, presenting as blood in the urine (hematuria), blood in the stool, or bleeding from the nose or gums.
Medical management focuses primarily on identifying and treating the underlying cause, as this is the only way to halt the cycle of abnormal clotting and bleeding. If sepsis is the trigger, immediate antibiotic administration is the priority; if an obstetric complication is the cause, removing the source of the procoagulant material is necessary. Supportive care is also provided to manage the life-threatening consequences of DIC.
Diagnosis is aided by laboratory tests that assess the state of the clotting system, often utilizing scoring systems. A key diagnostic marker is a significantly elevated D-dimer level, indicating that large amounts of fibrin clots have been formed and broken down. Other findings typically include a low platelet count (thrombocytopenia), decreased fibrinogen, and prolonged clotting times such as the Prothrombin Time (PT). Treatment may involve replacing depleted blood components, such as administering fresh frozen plasma to restore clotting factors or platelet transfusions for active bleeding.