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Disseminated Intravascular Coagulation

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Description: Disseminated intravascular coagulation (DIC) is a complex condition where widespread clotting occurs in the blood vessels, leading to both clotting and bleeding complications.
Type: Disseminated intravascular coagulation (DIC) is not a genetic disease. It is a serious condition that results from excessive activation of blood clotting in the blood vessels throughout the body, which can lead to severe bleeding and organ damage. DIC is typically associated with other underlying conditions such as severe infections, trauma, cancer, or complications during pregnancy.
Signs And Symptoms: In DIC, the underlying cause usually leads to symptoms and signs, and DIC is discovered on laboratory testing. The onset of DIC can be sudden, as in endotoxic shock or amniotic fluid embolism, or it may be insidious and chronic, as in cancer. DIC can lead to multiorgan failure and widespread bleeding.
Prognosis: Prognosis varies depending on the underlying disorder, and the extent of the intravascular thrombosis (clotting). The prognosis for those with DIC, regardless of cause, is often grim: between 20% and 50% of patients will die. DIC with sepsis (infection) has a significantly higher rate of death than DIC associated with trauma.
Onset: Disseminated intravascular coagulation (DIC) can have an acute or chronic onset. Acute DIC develops rapidly, often due to severe infections, trauma, or obstetric complications. Chronic DIC develops more slowly and may be associated with conditions like cancer or chronic inflammatory diseases.
Prevalence: The prevalence of disseminated intravascular coagulation (DIC) is not well-defined at a global level, as it often occurs as a complication of various underlying conditions such as sepsis, trauma, or cancer. It is considered relatively rare but can be significant in specific patient populations, such as those in intensive care units or with severe infections.
Epidemiology: DIC is observed in approximately 1% of academic hospital admissions. DIC occurs at higher rates in people with bacterial sepsis (83%), severe trauma (31%), and cancer (6.8%).

== References ==
Intractability: Disseminated intravascular coagulation (DIC) is a serious condition that can be difficult to manage due to its complex and multifactorial nature. It involves widespread clotting in the blood vessels, which can lead to multiple organ damage. The treatment focuses on addressing the underlying cause and managing symptoms, but the mortality rate is high, especially if the underlying cause is severe or not quickly identified and treated. Therefore, while not entirely intractable, DIC can be extremely challenging to treat effectively.
Disease Severity: Disseminated Intravascular Coagulation (DIC) is a serious and potentially life-threatening condition. It involves widespread activation of the body's clotting mechanisms, which can lead to both excessive clotting and severe bleeding. The severity of DIC varies depending on the underlying cause, but it often indicates a critical and advanced stage of an illness or injury, necessitating immediate medical intervention.
Healthcare Professionals: Disease Ontology ID - DOID:11247
Pathophysiology: Under homeostatic conditions, the body is maintained in a finely tuned balance of coagulation and fibrinolysis. The activation of the coagulation cascade yields thrombin that converts fibrinogen to fibrin; the stable fibrin clot being the final product of hemostasis. The fibrinolytic system then functions to break down fibrinogen and fibrin. Activation of the fibrinolytic system generates plasmin (in the presence of thrombin), which is responsible for the lysis of fibrin clots. The breakdown of fibrinogen and fibrin results in polypeptides called fibrin degradation products (FDPs) or fibrin split products (FSPs). In a state of homeostasis, the presence of plasmin is critical, as it is the central proteolytic enzyme of coagulation and is also necessary for the breakdown of clots, or fibrinolysis.In DIC, the processes of coagulation and fibrinolysis are dysregulated, and the result is widespread clotting with resultant bleeding. Regardless of the triggering event of DIC, once initiated, the pathophysiology of DIC is similar in all conditions. One critical mediator of DIC is the release of a transmembrane glycoprotein called tissue factor (TF). TF is present on the surface of many cell types (including endothelial cells, macrophages, and monocytes) and is not normally in contact with the general circulation, but is exposed to the circulation after vascular damage. For example, TF is released in response to exposure to cytokines (particularly interleukin 1), tumor necrosis factor, and endotoxin. This plays a major role in the development of DIC in septic conditions. TF is also abundant in tissues of the lungs, brain, and placenta. This helps to explain why DIC readily develops in patients with extensive trauma. Upon exposure to blood and platelets, TF binds with activated factor VIIa (normally present in trace amounts in the blood), forming the extrinsic tenase complex. This complex further activates factor IX and X to IXa and Xa, respectively, leading to the common coagulation pathway and the subsequent formation of thrombin and fibrin.The release of endotoxin is the mechanism by which Gram-negative sepsis provokes DIC. In acute promyelocytic leukemia, treatment causes the destruction of leukemic granulocyte precursors, resulting in the release of large amounts of proteolytic enzymes from their storage granules, causing microvascular damage. Other malignancies may enhance the expression of various oncogenes that result in the release of TF and plasminogen activator inhibitor-1 (PAI-1), which prevents fibrinolysis.Excess circulating thrombin results from the excess activation of the coagulation cascade. The excess thrombin cleaves fibrinogen, which ultimately leaves behind multiple fibrin clots in the circulation. These excess clots trap platelets to become larger clots, which leads to microvascular and macrovascular thrombosis. This lodging of clots in the microcirculation, in the large vessels, and in the organs is what leads to the ischemia, impaired organ perfusion, and end-organ damage that occurs with DIC.Coagulation inhibitors are also consumed in this process. Decreased inhibitor levels will permit more clotting so that a positive feedback loop develops in which increased clotting leads to more clotting. At the same time, thrombocytopenia occurs and this has been attributed to the entrapment and consumption of platelets. Clotting factors are consumed in the development of multiple clots, which contributes to the bleeding seen with DIC.Simultaneously, excess circulating thrombin assists in the conversion of plasminogen to plasmin, resulting in fibrinolysis. The breakdown of clots results in an excess of FDPs, which have powerful anticoagulant properties, contributing to hemorrhage. The excess plasmin also activates the complement and kinin systems. Activation of these systems leads to many of the clinical symptoms that patients experiencing DIC exhibits, such as shock, hypotension, and increased vascular permeability. The acute form of DIC is considered an extreme expression of the intravascular coagulation process with a complete breakdown of the normal homeostatic boundaries. DIC is associated with a poor prognosis and a high mortality rate.There has been a recent challenge however to the basic assumptions and interpretations of the pathophysiology of DIC. A study of sepsis and DIC in animal models has shown that a highly expressed receptor on the surface of hepatocytes, termed the Ashwell-Morell receptor, is responsible for thrombocytopenia in bacteremia and sepsis due to Streptococcus pneumoniae (SPN) and possibly other pathogens. The thrombocytopenia observed in SPN sepsis was not due to increased consumption of coagulation factors such as platelets, but instead was the result of this receptor's activity, enabling hepatocytes to ingest and rapidly clear platelets from circulation. By removing prothrombotic components before they participate in the coagulopathy of DIC, the Ashwell-Morell receptor lessens the severity of DIC, reducing thrombosis and tissue necrosis, and promoting survival. The hemorrhage observed in DIC and among some tissues lacking this receptor may therefore be secondary to increased thrombosis with loss of the mechanical vascular barrier.Activation of the intrinsic and extrinsic coagulation pathways causes excess thrombus formation in the blood vessels. Consumption of coagulation factors due to extensive coagulation in turn causes bleeding.
Carrier Status: Disseminated intravascular coagulation (DIC) is not a condition associated with carrier status, as it is not an inherited disease. Instead, DIC is an acquired disorder resulting from various underlying conditions such as severe infections, trauma, cancers, and other medical issues that trigger widespread activation of the clotting cascade.
Mechanism: Disseminated Intravascular Coagulation (DIC) is a complex condition characterized by systemic activation of blood coagulation, leading to the formation of blood clots throughout the body and eventually resulting in simultaneous bleeding due to consumption of clotting factors.

### Mechanism:
1. **Triggering Event**: DIC is often triggered by an underlying condition such as sepsis, severe trauma, cancer, or obstetric complications. These conditions lead to widespread endothelial damage or release of procoagulant substances.
2. **Coagulation Cascade Activation**: This trigger leads to the activation of the coagulation cascade, where procoagulant factors such as tissue factor are released into the bloodstream.
3. **Widespread Clot Formation**: The activation of the coagulation pathways leads to the formation of fibrin-rich clots in small and mid-sized blood vessels, consuming platelets and coagulation factors.
4. **Consumption Coagulopathy**: Due to the massive clot formation, the body's supply of platelets and clotting factors are depleted, leading to a paradoxical increased risk of severe bleeding.

### Molecular Mechanisms:
1. **Tissue Factor (TF)**: Endothelial damage or inflammatory cytokines induce the expression of TF, which is a primary initiator of the coagulation cascade by activating Factor VII.
2. **Thrombin Generation**: TF activates Factor X and, subsequently, prothrombinase complex which converts prothrombin to thrombin. Thrombin is a key enzyme that converts fibrinogen to fibrin, forming blood clots.
3. **Inhibition of Fibrinolysis**: In DIC, fibrinolysis – the process of breaking down clots – is inhibited. This is often due to increased levels of plasminogen activator inhibitor-1 (PAI-1).
4. **Inflammatory Cytokines**: Cytokines such as TNF-α and IL-6 can amplify the coagulation response by further enhancing TF expression and dampening the anticoagulant pathways.
5. **Natural Anticoagulant Pathways**: These pathways, including antithrombin III, protein C, and protein S, are overwhelmed or consumed during DIC, which exacerbates the hemostatic imbalance.
6. **Platelet Activation**: Concurrently, platelets are activated and aggregate, contributing further to the thrombus formation and subsequent consumption leading to thrombocytopenia.
7. **Endothelial Cell Dysfunction**: Endothelial cells can become prothrombotic under the influence of inflammatory mediators and lose their ability to provide an antithrombotic surface.

The interplay between coagulation, inflammation, and fibrinolysis in DIC results in a vicious cycle of continuous clot formation and breakdown, leading to multi-organ failure and severe hemorrhagic events.
Treatment: Treatment of DIC is centered on treating the underlying condition. Transfusions of platelets or fresh frozen plasma can be considered in cases of significant bleeding, or those with a planned invasive procedure. The target goal of such transfusion depends on the clinical situation. Cryoprecipitate can be considered in those with a low fibrinogen level. Treatment of thrombosis with anticoagulants such as heparin is rarely used due to the risk of bleeding.Recombinant human activated protein C was previously recommended in those with severe sepsis and DIC, but drotrecogin alfa has been shown to confer no benefit and was withdrawn from the market in 2011.Recombinant factor VII has been proposed as a "last resort" in those with severe hemorrhage due to obstetric or other causes, but conclusions about its use are still insufficient.
Compassionate Use Treatment: Disseminated intravascular coagulation (DIC) is a serious condition that involves widespread activation of the clotting cascade, leading to the formation of blood clots throughout the body and subsequent bleeding due to depletion of clotting factors.

1. **Compassionate Use Treatment**:
- In cases where standard treatments are not effective or available, some patients might be considered for compassionate use treatments. This can involve the use of investigational drugs or therapies that are not yet approved by regulatory agencies. The exact options would depend on the specific case and availability.

2. **Off-label Treatments**:
- **Recombinant Activated Protein C**: Although it was withdrawn from the market for sepsis-related DIC due to limited efficacy and safety concerns, in certain instances, clinicians might still consider its off-label use.
- **Tranexamic Acid**: Sometimes used in managing bleeding complications associated with DIC, despite not being specifically approved for this condition.
- **Antithrombin III**: Used off-label to replenish antithrombin levels, which can be beneficial in certain cases of DIC.

3. **Experimental Treatments**:
- **Novel Anticoagulants**: Investigational agents targeting specific parts of the clotting cascade are being studied in clinical trials.
- **Immunomodulatory Therapies**: There is ongoing research into immunomodulatory treatments that might help manage the underlying triggers of DIC, particularly in cases related to sepsis or severe infections.
- **Gene Therapy and Targeted Molecular Treatments**: These are in very early stages of research and are aimed at correcting underlying coagulation abnormalities.

Given the complexity and seriousness of DIC, treatments must be tailored individually, ideally within a clinical trial or under strict clinical supervision.
Lifestyle Recommendations: Disseminated intravascular coagulation (DIC) is a complex condition that involves widespread blood clotting and subsequent bleeding. Lifestyle recommendations may vary depending on the underlying cause and individual patient circumstances, but general guidelines include:

1. **Medical Management**: Regular follow-ups with your healthcare provider to monitor the condition.
2. **Healthy Diet**: Consuming a balanced diet to support overall health.
3. **Stress Management**: Practicing techniques such as meditation, deep-breathing exercises, and yoga to reduce stress levels.
4. **Avoiding Alcohol and Smoking**: These can exacerbate the condition and interfere with medications.
5. **Medications Compliance**: Taking medications as prescribed by your healthcare provider and discussing any side effects.
6. **Monitoring Symptoms**: Keeping track of any new or worsening symptoms and informing your healthcare provider promptly.
7. **Infection Prevention**: Practicing good hygiene and avoiding exposure to infections, as infections can precipitate or worsen DIC.

Always consult with a healthcare professional to tailor these recommendations to your specific needs.
Medication: Disseminated Intravascular Coagulation (DIC) is a complex condition that requires prompt medical attention. Treatment for DIC primarily focuses on addressing the underlying cause and managing symptoms. Medications and interventions commonly used include:

1. **Anticoagulants**: Low-dose heparin might be used in some cases to prevent further clotting.
2. **Blood Products**:
- **Platelet transfusions**: To treat low platelet counts.
- **Fresh frozen plasma**: To replace depleted clotting factors.
- **Cryoprecipitate**: To replace fibrinogen and other clotting factors.
3. **Supportive Care**:
- Intravenous fluids to maintain blood pressure and organ perfusion.
- Oxygen therapy for those with respiratory complications.

It’s crucial to treat the underlying cause of DIC, such as infections, trauma, or malignancies, to stabilize the patient's condition.
Repurposable Drugs: Disseminated Intravascular Coagulation (DIC) is a serious condition involving widespread blood clotting and bleeding. There are a few existing drugs that could potentially be repurposed for treating DIC:

1. **Heparin**: An anticoagulant that can help manage the clotting aspect of DIC, though its use is controversial because it may exacerbate bleeding issues.
2. **Tranexamic Acid**: An anti-fibrinolytic that could help control hemorrhage.
3. **Recombinant Human Activated Protein C (rhAPC)**: Previously used in sepsis, it has anticoagulant, anti-inflammatory, and cytoprotective properties which could be beneficial in DIC.
4. **Fresh Frozen Plasma (FFP)**: Provides clotting factors and can help restore coagulation balance.

Close monitoring and supportive care are essential when using these therapies due to the complex and variable nature of DIC.
Metabolites: Disseminated intravascular coagulation (DIC) is a complex condition that involves widespread activation of the clotting cascade, leading to the formation of clots in the small blood vessels. This can cause multiple organ damage and bleeding due to the consumption of clotting factors. Metabolites involved in DIC can include fibrin degradation products (FDPs), D-dimers, and other markers of coagulation and fibrinolysis. These are measured to assess the extent and severity of the condition.
Nutraceuticals: There is limited evidence to support the use of nutraceuticals in the management of disseminated intravascular coagulation (DIC). Treatment typically focuses on addressing the underlying cause, supportive care, and managing coagulation abnormalities with conventional medical interventions. Before considering any alternative therapies, it is essential to consult a healthcare professional.
Peptides: Disseminated Intravascular Coagulation (DIC) is a serious condition characterized by widespread activation of the coagulation pathways, leading to the formation of blood clots in small blood vessels throughout the body. This can result in multiple organ damage and is often associated with severe infections, trauma, or other medical conditions.

**Peptides:** In the context of DIC, peptides may refer to bioactive molecules involved in coagulation and inflammation pathways. These peptides could include coagulation factors, such as fibrinogen-derived peptides, or other signaling molecules like cytokines that play a role in the inflammatory response.

**Nan:** This term is not directly related to DIC but may reference nanotechnology or nanoparticles in a broader medical context. While not currently standard treatment, research is exploring the use of nanoparticles for targeted drug delivery or diagnostic purposes in coagulation disorders, including DIC. This includes developing nanoparticles that can deliver anticoagulants or anti-inflammatory agents directly to sites of clot formation or inflammation.