Introduction
Disseminated intravascular coagulation is a condition that involves clotting factors. In this case, clotting factors have been interrupted in a way that causes them to overreact and sometimes become unavailable for normal clotting mechanisms. It is considered a secondary diagnosis because the complication is created by a preexisting condition. A preexisting condition introduces a procoagulant into the bloodstream and causes the blood to coagulate excessively. Coagulation is the process of clot formation. Systemic coagulation produces excessive blood clots in the blood stream. When blood clots are formed in the vascular system, they can travel throughout the body via the circulatory system and minimize circulation to organs. Thromboses can also be lodged inside of blood vessels, travel to the lungs, extremities or even to the brain.
When the body manifests disseminated intravascular coagulation rapidly it can cause severe bleeding. The hemorrhaging may be internal or from a small wound that normally would not bleed as much. This is because when coagulation occurs acutely the normal compensatory mechanisms of homeostasis are quickly overwhelmed and the inability to clot, coagulopathy, becomes a new concern. Clotting factors are essentially "tied up", causing excessive bleeding and an ironic change in the blood’s ability to clot. This is a life-threatening condition which could lead to bleeding into the organs. When disseminated intravascular coagulation occurs
Leads to a reduced ability to form blood clots due to a decreased number of platelets.
The Biggest risk associated with idiopathic thrombocytopenic purpura is bleeding, especially bleeding into the brain (intracranial hemmorrhage), which can be fatal. Major bleeding is rare with ITP,
Venous thrombosis is a multifactorial disease. In the majority of thrombosis patients a risk factor is not detectable. Virchow's triad refers to three primary influences for thrombus formation, endothelial injury, stasis, turbulence or abnormal blood flow, and blood hypercoagulability (Kyrle, 2009). A shift in balance between procoagulant and anticoagulant of the endothelium is responsible for thrombotic state (Kyrle, 2009). Endothelial injury is the physical loss of endothelium leading to exposure of subendothelial extra-cellular matrix, adhesion of platelets, release of tissue factor, depletion of PGI2 and plasminogen activators (Kumar, 2010). Abnormal blood flow refers to turbulence that causes endothelial injury, which is a major influence
McCartney CA, Paredes N, Chan AKC. Disorders of coagulation in the neonate. In: Hoffman R, Benz EJ Jr, Silberstein LE, Heslop HE, Weitz JI, Anastasi JI, eds. , Hematology; basic principles and practice 6th ed. Philadelphia, PA: Elsevier Saunders, 2012 chap. 152
Both conditions increase coagulability. Atherosclerosis increases platelet function by encouraging aggregation and adherence. Immobility, in contrast, contributes to hypercoagulability by increasing procoagulation factors.
This organ system has a number of functions namely, to keep a constant body temperature as well as to ensure coagulation occurs specifically at the site of injury, as well as to ensure no added blood loss occurs to cause life-threatening effects. This process of blood coagulation is explained in three interconnected phases. In the first phase, the enzyme thrombokinase is activated due to the damage of tissue and the breaking down of platelets. Prothrombin is converted into thrombin by the disintegration of the thrombocytes, electrically charged calcium ions and other coagulation factors, as well as the blood activator and tissue activator which become involved in the coagulation process. The second phase includes production of the thrombin that transforms fibrinogen in the blood plasma into fibrin. The thrombus (or blood clotting) is formed by a fibrilliform mesh that encloses the blood cells. Lastly, the third phase, which takes place as retraction occurs of the fibres of the fibrin mesh. Solidification of the fibrous mesh takes place which closes the defect in the vascular wall. Coagulation is then followed by fibrinolysis (re-dissolution of the clot).
Disseminated intravascular coagulation (DIC) is a serious problem involving abnormal clotting of blood throughout the body. Normally, when you get cut, special proteins help your blood clot at the injury site. In DIC, the protein factors that control blood clotting become abnormally active. Small blood clots form that can clog up blood vessels and can cut off the blood supply to important organs, such as the liver, brain, or kidneys. As DIC worsens, the blood does not clot very well and serious bleeding can occur. This can be life-threatening. DIC can be sudden onset (acute) or long-term (chronic).
After injury Platelets adhere to the site of injury, then platelet gets activated and aggregated followed by activation of coagulation cascade and formation of clot.28,29
Blood clots are a serious side effect when it comes to taking the pill. Certain pills may cause or increase the risk even more. According to Planner Parenthood "The progestin in YAZ, Gianvi, YASMIN, Ocella, Syeda, and Zarah, Beyaz, and Safyral may be linked to a higher risk for blood clots than other birth control pills" It is a good chance doctors will advice women to stay away from these. Anything that can increase the risk of blood clots should be avoided because blood clots are very serious and dangerous. The most familiar place for the clot the leg or lung. The pills do not cause the clot it can higher the chances of getting one. "For the average woman taking birth control pills, the absolute risk of a blood clot is very small: Only 1
(Karmiova, 2001) and is predictive of subsequent multiple organ failure, infection and than eventually death in these patients. These conditions have many features common with sepsis. Blood concentrations of various cytokines, soluble receptors and endotoxins increase within as early as 3 hours after cardiac arrest, the magnitude of these changes is associated with the outcome. Activation of blood coagulation without adequate activation of endogenous fibrinolysis is an important pathophysiological mechanism that may contribute to microcirculatory reperfusion disorders (Böttiger, 1995). For patients that undergo CPR and achieve ROSC, their coagulation/anticoagulation and fibrinolysis/antifibrinolsis systems are activated. Anticoagulant factors such as antithrombin, protein S and protein C are decreased and this decrease is associated with transient increases in endogenous activated protein C after resuscitation (Adrie,2005). The stress of total-body oxygen debt also affects adrenal production and function. Although patients have increased plasma cortisol levels they have a relative adrenal insufficiency defined as failure to respond to corticotrophin. This failure to respond causes the adrenal cortex to not be stimulated to secrete the hormones necessary to respond to stress.
You mentioned hemophilia so I just wanted to explain what it was. Hemophilia is an inherited disease that affects the clotting process of your blood. Therefore, if you have hemophilia you do stand a chance of sever bleeding if you incur an injury or cut. There is a protein that is called clotting factor that a person might have little or none at all. It is a protein used for blood clotting that helps blood platelets stick together. (NIH
Hemophilia is a rare disorder when blood doesn't clot normally because it is short on sufficient blood-clotting proteins. Deep bleeding inside the body is big concern especially in the knees, ankles and elbows. The internal bleeding caused from this can damage the organs and tissues of the body and may be life threating. When a person without Hemophilia is injured, a system of procedures happens to make the blood turn from liquid to solid to clot the wound and make the blood flow stop. Platelets, which are cells found in the blood, combine together to form a clot at the site of bleeding. The platelets hold an enzyme that causes fibrinogen to change to fibrin which is a solid substance that doesn’t liquefy. The fibrin goes to the area of injury
overproduction of megakaryocytes in the bone marrow. This means the platelets number increase in the peripheral blood and it is called Thrombocythemia. This disorder is called essential because the increase in platelets number is a distinctive problem of the blood cell production in the bone marrow (Rumi et al., 2014).
These disorders occur as a result of cellular structure imbalances in the body and can cause blood clots, swelling, and excessive bleeding.
Most bleeding episodes in hemophilia are not considered “life-threatening”. There are however, some areas of the body, or some witnessed events that should be treated as an emergency. It is important that people with hemophilia receive factor and seek medical attention immediately if they witness or suspect a bleed to any of the following areas: head, eye, neck, stomach, spine, or hip (“hemophilia” 2002).