Introduction
Disseminated Intravascular Coagulation often abbreviated as DIC is a condition that involves procedural activation of blood coagulation leading to the production and deposition of fibrin in an individual’s body (Cate, Timmerman & Levi, 2009). This condition often prevents blood of the affected individual from clotting as expected. As such, the affected person tends to experience blood clotting problems; a condition that affects the flow of blood and causes multiple organs failure.
Disseminated intravascular coagulation (DIC) is defined as an acquired syndrome that is characteristic of intravascular coagulation activation leading to the loss of localization, as a result of diverse causes (Letsky, 2001). Slofstra, Spek and Cate (2003) asserted that disseminated intravascular coagulation does not refer to a particular illness, but a condition that is secondary to other disorders within the body. DIC results from several clinical conditions such as sepsis, organ destruction, severe transfusion, malignancy, among others.
Normal Physiology of Homeostasis
Cate,Timmerman and Levi (2009) pointed out that organ systems are responsible for maintaining body homeostasis. For the body to function effectively, the organ systems ensure that there is a stable internal environment. As such, the body can adjust to any internal environment. In the case of disseminated intravascular coagulation, an individual suffers from organ failure resulting from lack of proper blood clotting. However, the circulatory system counters such conditions by producing blood platelets to enhance fast clotting. Several pathologic factors change the normal coagulation (Letsky, 2001). Normal coagulation occurs primarily in overlapping phases (Levi, 2007).
Whenever any injury is detected in the body, platelets are released to the injured site through the help of a series of enzymes. However, antithrombotic control systems ensure that only the injured part is occupied by the platelets clot (Slofstra, Spek & Cate, 2003). In case of excessive deposition of clots, fibrinolysis removes the deposited debris. During normal homeostatic conditions in the body of any individual, fibrinolysis and coagulation balance help to maintain the body (Levi, 2007). When coagulation is activated, fibrinogen is converted to fibrin by the help of thrombin. After the activation of blood coagulation, the released fibrin results in microvascular thrombi in several body organs.
Such a condition eventually leads to multiple dysfunction syndrome. The activated fibrinoltyic system leads to the generation of plasmin, a useful substance for lysis fibrin clots. If the activation of coagulation proceeds, the body consumes and exhausts platelets and coagulation protein. If the process persists, an individual might experience severe bleeding. Further derangement of the fibrinolytic system can led to the formation of intravascular clots although in most cases, the persistence of the problem leads to severe bleeding. For this reason, individuals suffering from disseminated intravascular coagulation (DIC) have a high chance of having bleeding and thrombotic problem that is likely to complicate the initial treatment of DIC.
Pathophysiology
The generation of TF-mediated thrombin, impaired fibrin removal, dysfunctional physiologic anticoagulant, and inflammatory activation are the major mechanisms responsible for the hematologic derangements evident in disseminated intravascular coagulation (Levi, 2007). The normal physiology of the body is largely affected by the disseminated intravascular coagulation. Whenever, the clotting flow is activated, blood clots are formed in major small blood vessels within the entire body of the affected individual.
Such a condition allows the circulation of thrombin that leads to fibrinogen cleavage. The cleaving of fibrinogen is responsible for numerous fibrin clots within the blood (Yu, Nardella & Pechet, 2000). Fibrin clots trap platelets in the blood resulting to larger clots and hence causes thrombosis. Formation of such blood clots affects the normal flow of blood within the vessels. Usually, all body organs depend on the circulatory system for supply of blood. As such, major body organs are negatively affected following the alteration of blood flow within the body tissues.
Additionally, the coagulation process leads to consumption of the available blood platelets, which interrupts the normal process of clotting and leads to severe bleeding at various body sites (Slofstra, Spek & Cate, 2003). In disseminated intravascular coagulation, fibrinolysis and coagulation processes are deregulated leading to extensive clotting that is accompanied by excessive bleeding. The pathophysiology of disseminated intravascular coagulation is often the same regardless of the factors responsible for the DIC. According to Yu, Nardella and Pechet (2000), the body mediates the effects of disseminated intravascular coagulation by releasing tissue factor (TF), a form of trans-membrane glycoprotein.
From the discussion above, it is evident that disseminated intravascular coagulation is a very severe condition that affects the normal functions of the body. Even though cases of disseminated intravascular coagulation are rare, the condition is life-threatening when it affects any individual. Its severity is attributed to the fact that the DIC affects the normal flow of blood by preventing blood from clotting normally. As such, DIC leads to dysfunction of numerous body organs such as the lungs, liver, kidney, among other vital organs. However, Levi (2007) pointed out that the organ systems in the human body are very important in ensuring homeostasis balance. For this reason, body enzymes and other substances such as blood platelets help in countering the effects of DIC.
References
Cate, H., Timmerman, J. J., & Levi, M. (2009). The pathophysiology of disseminated intravascular coagulation. Thromb Haemost, 82(2), 713-717.
Letsky, E. A. (2001). Disseminated intravascular coagulation. Best Practice & Research Clinical Obstetrics & Gynaecology, 15(4), 623-644.
Levi, M. (2007). Disseminated intravascular coagulation. Critical care medicine, 35(9), 2191-2195.
Slofstra, S. H., Spek, C. A., & Cate, H. T. (2003). Disseminated intravascular coagulation. The Hematology Journal, 4(5), 295-302.
Yu, M., Nardella, A., & Pechet, L. (2000). Screening tests of disseminated intravascular coagulation: guidelines for rapid and specific laboratory diagnosis. Critical care medicine, 28(6), 1777-1780.