Early Coagulopathy in Trauma Patients - Literature review Example

Running Head: COAGULOPATHY IN EARLY TRAUMA Title: Institution: Course: Date: Introduction The term Coagulopathy is used to refer to a condition where there is excessive bleeding or hemorrhage that does not stop easily. Coagulopathy is associated with trauma because trauma victims tend to suffer from uncontrollable bleeding. For every ten deaths in the world, one is caused by trauma. About 39% of trauma victims die from Coagulopathy. Bleeding resulting from Coagulopathy is normally very difficult to control. Several things are known to cause Coagulopathy in trauma patients; Engelman et al (1996) .They are inclusive of dilution and consumption of coagulation factors and blood cells. It also results from improper functioning of coagulation systems and blood cells. “The interplay between, acidosis, hypothermia, and progressive Coagulopathy called ‘lethal triad’ often results in exsanguinations. This triad is responsible for many deaths in trauma conditions and should be broken or avoided in order to save the patient’s life. A therapy that replaces the components of the blood is being used currently for the management of Coagulopathy. However replacement has a certain limit beyond which it cannot be taken. Transfusion of platelets shortly after injuries raise the possibility of infection and may lead to failure of the organs; (McLeod 2003).Coagulopathy and excessive bleeding control strategies can reduce the need for transfusion of blood and therefore improve the clinical results of trauma patients. Trauma causes five million deaths every year with one million of the deaths occurring in Europe. Fatal bleeding in trauma victims results from coagulopathy and vascular injuries. When main blood vessels are injured surgery is required; (Lynn 2002). However embolization of arteries is normally useful in controlling bleeding in all patients even in those with multiple trauma. When diffuse bleeding is coagulopathy related it becomes so hard to manage. Coagulopathy is caused by many interrelated factors such as ‘ consumption and dilution of coagulation factors and platelets, dysfunction of platelets and the coagulation system, increased fibrinolysis, compromise of the coagulation system by the infusion of colloid, hypocalcaemia and disseminated intravascular coagulation like syndrome.” Engelman et al (1996). Medical remedy for trauma patients who have excessive bleeding is done by a lot of colloid and crystalloid being infused before the transfusion of red cells. Nevertheless red blood cell concentrates have very little quantities of coagulation factors and platelets. Consequently, red blood cell transfusion may increase transportation of oxygen but cannot replace lost platelets and coagulation factors and the end result can be coagulopathy; Martinowitz et al (2001). “Bleeding associated with coagulopathy is corrected by the transfusion of Fresh Frozen Plasma, coagulation factor concentrates, platelets and cryoprecipitate if available. The coagulation factor concentrates used are fibrinogen and pro-thrombin complex concentrates.” In cases where coagulopathy occurs together with acidosis and hypothermia sufficient replacement cannot stop the bleeding. The resultant effect is normally exsanguination. Coagulopathy is known to come immediately after the injury and it can cause death on its own; Watts et al (1998).If coagulopathy is controlled early enough death in patients suffering from severe trauma is reduced considerably. Multiple failures of organs and infection cause problems in people who happen to move on after the injury. The transfusion of red blood cells has been suspected to increase the level of ‘multiple organ failure’ and ‘post injury infection.’ As a corrective measure the red blood cell transfusion should be reduced to ensure lowered complications such as multiple ‘organ failure’ and improved outcome; McLeod (2003). Pathophysiology of coagulopathy in trauma Haemostasis process When a blood vessel is injured there follows interactions between coagulation proteins, subendothelial matrix and platelets. Usually, the endothelial cells covering the inside wall in the blood vessel bars the subendothelia matrix together with tissue factor from meting the coagulation proteins and circulating proteins. An injury in the blood vessel breaks the organization of the endothelial lining and in the process the subendothelial matrix is exposed. When platelets stick on the subendothelial matrix they become activated and form plugs. The plug operates as a surface for catalysis where coagulation proteins are recruited and activated. The process of coagulation is optimized; (Martinowitz 2001). The process of coagulation begins with activated factor VII being bound on the bare tissue factor which begins the coagulation when it activates factors IX and IX. Factor V is activated by factor IX. Factor V when activated it turns pro-thrombin into thrombin. Only little quantities of thrombin are created which are inadequate to turn fibrinogen into fibrin. The creation of thrombin is increased by a number of feedback mechanisms. “Initially, the production of activated factor VII grows with activation of factor VII attached to tissue factor by activated factors VII, IX, and X.” Armand (2003) In the second level thrombin produced makes factors VII, IX and X. After that thrombin produced does the activation of factors V and VIII and the co factors responsible for quickening the activation of pro-thrombin as well as factor X. Thrombin changes factor X into an activated state and in the process it increases production of factor IX. When large quantities of activated factor X are produced from factors IX and FVIII it becomes possible for enough quantities of thrombin are perpetually produced to change fibrinogen into fibrin and thus a clot is formed; Lynn et al (2002). In the last step of coagulation, factor VIII is activated by thrombin to activated factor VIII. This factor then forms cross-links in the soluble monomers of fibrin into a strong clot of fibrin. “In addition, thrombin activates the thrombin-activatable-fibrinolysis inhibitor which protects the clot from premature fibrinolysis.” There are many inhibitors and proteins that prevent coagulation which regulate haemostatic systems. The system is also regulated by the fibrinolytic process; Watts et al (1998). When there is a balance in operations the mentioned processes enables the clot formed form fibrin to prevent further bleeding and consequently the broken vessel is repaired and the blood flow maintained. Excessive bleeding in major trauma patients sometimes overwhelms the coagulation process and the end result is coagulopathy, bleeding that cannot be controlled and exsanguination. This happens even in people with formerly normal haemostasis; Gando et al (1992). Uncontrollable bleeding may be experienced when the vascular damage is greatly pronounced. Otherwise the mere failure of coagulation factors to take their positions can result in excessive bleeding. Consumption coagulopathy “The pathogenesis of coagulopathy in patients with trauma is complex.” The exact cause is hard to know but it is thought to be resulting from many factors. The damage of tissues, shock and anoxia make the coagulation system active which also activates fibrinolysis. When fibrinolytic and coagulation systems are activated normally the out come is the consumption of coagulation factors and platelets. More bleeding results in increased depletion of platelets and coagulation factors from the blood; McLeod (2003) Increased fibrinolysis Tests done in the laboratory have proved that there exists both hyperfibrinolytic and hypofibrinolytic states in patients with trauma. The condition of the injury and the time taken between the injury and time of assessment of fibrinolytic activity determines the fibrinolytic status of a trauma patient. Fibrinolytic activity is known to increase shortly after trauma. It comes back to normal within 24 hours if the injury was mild or moderate. If the injury is a major one it remains high. Fibrinolytic activity is elevated if hypothermia is present; Martinowitz et al (2001). Hypothermia has been observed to occur in most cases if the injury or dmage to blood vessels is big. Hypothermia-induced coagulopathy If a trauma patient who does not have already existing disease or bad head injury there are factors that can put him at risk in coagulopathy that can cause death. “These factors are: the severity of injury >25, systolic blood pressure Read More