Disseminated intravascular coagulation (DIC) is one of the most important and common acquired disorders of haemostasis. DIC is a disorder that mainly affects the blood clotting cascade. If the mechanisms of blood clotting are activated inappropriately, it will result in this disorder. This disorder can sometimes be seen as the end process in cancers and can be short or long term. DIC can lead to small clots being formed in the blood vessels which lead to these small clots, consuming platelets and coagulation proteins. This means the coagulation process is disrupted and abnormal bleeding occurs from the skin. So, the blood clotting factors are used up and therefore are unavailable for areas with actual injury. DIC can be seen in acute or chronic forms and can lead to multiple organ failure which could lead to death (Key, N,. et al 2009).
In normal haemostatic conditions, the body regulates the balance of fibrinolysis and coagulation. DIC does not just relate to a specific disease but is usually associated with many other pathologic conditions. An example is snakebite, where it will result in endothelial damage and a direct activation of coagulation by the venom (Saba, H, I,. 2005). The common causes of DIC are infections, malignancy, major trauma, connective tissue disorders and incompatible blood transfusion. A common infection is septicaemia.
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The pathophysiology of DIC involves the coagulation cascade being activated which produces thrombin. Thrombin then converts fibrinogen to fibrin which is the final stage of haemostasis. Plasmin is also produced via the activation of the fibrinogen system, which then lyses fibrin clots. This is important as plasmin is a vital proteolytic enzyme for coagulation and is also critical to the breakdown of clots. Fibrin degradation products (FDP's) are then produced by the breakdown of fibrin and fibrinogen.
There are many different anticoagulation mechanisms that can be disabled by consumptive coagulopathy. One critical mediator of DIC is the release of tissue factor (TF). The TF binds with coagulation factors which triggers the intrinsic and extrinsic pathways. With acute DIC, clotting factors and platelets get consumed more rapidly than they can be replenished. This can result in server bleeding and can be fatal. Chronic DIC develops slower and is associated with blood clots forming rather than bleeding. The most common cause of chronic DIC is cancer (Bick RL, 1998).
The presentation of DIC varies widely. As organ failure and bleeding are the two most common signs of DIC, the ratio of thrombin against plasmin can determine whether they are predominant in a patient. DIC can be caused by many serious disorders and depends on it being acute or chronic. The acute events can lead to depletion of platelets, intravascular coagulation and bleeding. These acute patients will show signs of multiple organ failure and very quickly progress with excessive bleeding because their factors, proteins and platelets get consumed. The disorder is spread throughout by micro deposits of fibrin which then initiates fibrinolysis (Fischbach, F., Dunning M, B., 2009).
There are a large number of symptoms for acute DIC, and most of them are related to blood clots around the body in vital areas. For example blood clots in the brain will present signs of headaches, dizziness and trouble speaking. In chronic DIC, the platelets and clotting factors get used up by the increased clotting therefore substantial internal and external bleeding occurs.
Chronic DIC normally results in excess of coagulation products and venous thrombosis. DIC is difficult to assess solely based on symptoms and should be recognized as early as possible to ensure survival. Specific systemic signs of DIC include hypoxia, fever and hypotension but the problem with these signs is that it could be for the disease that's caused the DIC for example sepsis. Even more specific signs can be cyanosis or severe bleeding from specific sites like epistaxis. Okajima et al (2000) suggested that 77% of patients with infections and DIC resulted in organ failure, while patients with obstetric disorders and DIC had a prevalence of organ failure less than 30%. A physical examination of a patient with DIC will show signs of purpura, oliguria and pulmonary edema. Purpura is caused by bleeding underneath the skin and can result in red discolouration of the skin as seen in this picture:
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Now, the laboratory investigation consists of many tests as there is no test specific to DIC. The reason for this is that most tests confirm the bleeding problem but only a few can identify the activation of the pro-coagulant system. So, a range of laboratory tests with the clinical condition of the patient can be used as an indication of DIC. Two substances which are always lower in the presence of DIC is the fibrinogen level and platelet count. A peripheral blood smear examination can be performed which should show mainly schistocytes and other characteristics. Here is a blood smear off a DIC patient showing a schistocyte:
The schistocytes are frequently found in DIC but are non-specific and can help in the diagnosis of DIC. They become fragmented parts by moving past the thrombus as seen in the picture above (Levi M,. Ten Cate, H,. 1999).
There are two accurate tests which are newly developed, called the D-dimer test and the FDP assay. An increased number of FDP's is found where clot formation and lysis occurs. The production of D-dimers is produced by plasmin interacting with the cross linked fibrin. These tests have been proved that they are efficient and specific to DIC (Bick RL, 1998). Levi M and Ten Cate H (1999) suggested that by investigating into the specificity and sensitivity of DIC, a combination of D-dimer tests and FDP assays would give the most rapid and specific response to DIC.
There are a number of other tests that can be performed that give an indication of DIC. Coagulation therapy can be used to show a prolonged prothrombin time (PT) and activated thromboplastin time (APTT). In mild cases of DIC, the AP and APTT are normal with just an increase of coagulation factors and platelets. With severe cases these two tests are prolonged and the fibrinogen level rapidly reduced.
If bleeding can be seen on the patient or if they need invasive procedures, the factor deficiencies and thrombocytopenia can be corrected with the addition of coagulation factors and platelets. If the platelet count is lower than 20K then platelet addition is required. When patients have less than 50K of target fibrinogen, coagulation factor should be given or even cryoprecipitate (Fischbach, F., Dunning M, B., 2009).
The management of patients is very important as it means prevention of the loss of platelets and clotting factors, therefore rescuing patients from DIC related bleeding complications. One example of an important specific therapy for the management of patients is the use of heparin. Heparin is a strong antithrombotic agent and its function is to block the activity of thrombin and therefore prevent additional coagulation. It has been successful in some cases of chronic DIC and is normally administered in low doses. Great caution needs to be taken with the use of heparin as it induces bleeding. During heparin therapy, the thromboplastin time has to be monitored and if the patient starts to bleed, the therapy should be immediately stopped. When this occurs, the addition of platelets or fresh frozen plasma will help to stable the patient (Carey MJ, Rodgers GM, 1998). Before heparin is used on the patient, the antithrombin III (ATIII) levels must be above 80% to enable the heparin-antithrombin complex to be formed.
Activated protein C (APC) is another example where it inactivates factors Va and VIIIa which results in a decrease of thrombin production. It can also be useful as an anticoagulant and as an anti-inflammatory and therefore reduces D-dimer in patients with sepsis. Aoki N, et al (2002) investigated into the comparison between the use of APC against heparin, and they found that in the APC patients, the bleeding reduced significantly. The mortality rate also halved from 40% to 20%. The APC commercial product used globally is called Xigris. Lots of development is going into these therapies and they can prove vital to a patient.
Research showed (Toh, CH,. 2001) that antifibrinolytic drugs are used only in severe cases as they can be fatal. These drugs won't be used by doctors before they look at the outcome in using heparin and other therapy first. They can help with severe bleeding, in combination with heparin, but can easily lead to thrombosis. A couple of examples of these drugs are aminocaproic acid and tranexamic acid.
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Another new drug called activated factor VII, has the ability to compensate for deficiencies of factor VII and factor VIII. Martinez J, et al (2005) showed in their study that 15 of the 18 patients stopped bleeding with the addition of this new drug. The problem with this drug is it could induce thrombosis, so more research is required with this drug. There are many other examples for the management of patients for example, coagulation modulator therapy, tissue factor pathway inhibitor and thrombomodulin.
In conclusion, DIC is a coagulation disorder and is mainly seen with intensive care patients. It is a symptom of an underlying disease, and the pathophysiology of the illness is what determines the clinical presentation of DIC. Large amounts of thrombin is formed which activates the tissue factor pathway. This can ultimately lead to thrombosis and eventually death which is due to the consumption of clotting factors. The development of different treatments and management schemes is on-going, using the patient's clinical information and coagulation therapy tests. The best management of a DIC patient focuses on the treatment of the underlying disorder.