Coagulopathy refers to a blood clotting disorder whereby the body is unable to respond to an injury by clotting the blood to reduce the level of blood loss. The blood clotting mechanism is very crucial in the body and it is affected by the Thrombocytes (Brohi, Singh, Heron & Coats 2003). There is a number of blood clotting disorders that result in the malfunctioning of the thrombocytes. These disorders include haemophilia, disseminated intravascular coagulation, the thrombocytopenia, Hypoprothrombinemia among others (Denninger & De Prost 2007).
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According to James, Bradley, Christine and David, (2007), the coagulation traumatic effect in the body can be evaluated depending on a number of key factors. They include the severity of the injury on the patient, hypothermia, thermographic shock among others. This prompted a number of theories to be formulated so as to come up with a viable explanation as to what are the real causes of coagulation trauma. These theories include the platelet alteration theory, the enzyme inhibition theory and fibrinolysis (Denninger.& De Prost, 2007). The three theories have been used side by side to come up with the best explanation of what actually causes coagulation trauma in case of an injury. The interrelation in the use of the three theories will help in identification as to whether there is a consistency in the factors that are attributed as playing the key role in defecting the blood clotting process in case of an injury (Bernard and Buist 2009). The study therefore will focus on discussing intensively each of the three theories and identify if there is a consistency in the factors that are attributed to causing coagulation trauma explained in each.
The platelet alteration theory
Platelets are very important components of the blood in any mammal. In case an animal sustains an injury, the coagulation process is activated. The platelets form a mesh like a wall that attracts the red blood cells. On exposure of the red blood cells to the atmosphere, they form a cast that prevents continued blood from the injury sustained (James, Bradley, Christine & David, 2007).
However, the platelet activation process in case of a severe injury does not follow the normal procedure of the supersonic conversion of fibrinogen to fibrin due to some alternations exhibited by the platelets. This abnormal behaviour of the platelets is explained using the platelet alteration theory of coagulation traumatic theories. The theory holds that platelets themselves do not initiate the coagulation process. Therefore, platelet alteration results from physio-chemical alterations. These alterations are either genetically acquired or are acquired from a deficiency in one of the proteins that make up the platelets or a malfunction of the proteins (Bernard and Buist 2009). The most common causes of platelet defects that cause coagulopathy are explained below as follows: –
Haemophilia A and B
Haemophilia A and B are hereditary diseases. The haemophilia disease is manifested dominantly in males as they get their x chromosomes from their mothers. However, at times non-random inactivation of x chromosomes together with overexpression of its coding for the genes that carry haemophilia may cause coagulopathy in females (Betty & Paul 2004). This happens in rare cases as the haemophiliac genes are carried mainly by the females. Haemophilia is caused by a deficiency in the clotting factors either VII or IX. The deficiency of factor VII causes haemophilia A while haemophilia B is caused by factor IX deficiency. The absence of these crucial elements in the platelets results in the inability of the blood to clot and prevent blood loss. However, if a person is haemophilic doesn’t ascertain the total absentia of the clotting factor in the person but these factors may be present but in very low counts in the blood.
Trauma patients of haemophilia experience hemarthrosis. Hermathrosis refers to bleeding in the joints resulting in painful stiffening of the joints and if the bleeding is severe, it may cause disability or hematuria and gastrointestinal bleeding. The bleeding in haemophiliac persons varies and the severity of it depends on the clotting factor levels in the blood in terms of deficiency. In haemophilia A the levels of clotting factor VIII ranges between 0 to 30 per cent and this is considered normal in the medical fraternity. When this happens, the platelet count, prothrombin time and bleeding time are all normal (Denninger & De Prost 2007). Partial thromboplastin time is prolonged. In haemophilia B the clotting factor IX levels are usually low and prothrombin time is prolonged as compared to haemophilia A.
Clotting factor deficiency
Clotting factors such as fibrinogen, II, V, VII or X, though uncommon, may lead to problems in coagulation mechanisms like those experienced in haemophilia. The deficiency of these factors causes over bleeding. They can be detected in a person early in their lives whereby this situation can be rectified permanently or temporarily (Mardel, Saunders, & Allen, 2009).
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It is commonly used for the treatment of blood clotting in blood vessels or in its prevention. Since anticoagulant drugs such as heparin or warfarin block or stop the clotting process, they can cause coagulopathy if they are present in the blood. Blood thinners may also exacerbate the risk since such thinners block the clotting process of the platelets. Therefore, the physicians who make diagnoses should extremely be cautious when they are treating this problem of blood clotting as the medication meant to inhibit clotting, can at times result in coagulopathy (Risberg, Medegard, Heideman, et al,.(2008)
Von Willebrand disease
Clotting factors require platelets as a reaction surface. Platelet’s rail themselves on the wall of the blood vessel at the injured site. This is facilitated by the von Willebrand factor to form a mesh like wall that traps the red blood cells forming a cast that prevents further blood loss. Low levels of van Willebrand factor causes poor clotting or delayed clotting (Paran, Gutman & Mayo, 2005).
Vitamin K deficiency
Vitamin K is a very important nutrient that is required in the human body at low levels. Three types of vitamin K are: phylloquinone, menaquinone and menadione (Paran, Gutman & Mayo, 2005). The vitamin K deficiency may be caused by a number of factors which may be as a result of inheritance of a rare bleeding disorder due to a dysfunction of clotting factors II, VII, IX and X. For the process of coagulation to take effect, activation of these four factors is needed in the presence of vitamin K, When this reaction doesn’t take effect as it should, the clotting process is blocked and the blood clot does not form. This is an autosomal recessive disorder that affects both males and females. Both the parents must possess the defective gene for it to be passed to their offspring. It can be acquired also as a result of liver disease, bowel disorders, and vitamin K deficiency in the diet and also due to blood-thinning medication (Ryan, Cortez, Dick, & Pusateri, 2006). Newborn babies may sometimes have a temporary form of vitamin K deficiency, but this can be treated with the administration of supplements after birth.
Platelet dysfunction refers to the inability of the thrombocytes to clot and form mesh like strands that prevent loss of blood. There are three types of platelet dysfunction (Osterud & Bjorklid, 2006). These range from the commonly acquired ones to genetic ones. Acquired platelet dysfunction may be a result of blood plasma inhibitory substances. This dysfunction is mostly seen in diseases such as uraemia, pernicious anaemia, infused dextrin and liver diseases (Rajek, Greif & Sessler.2007).
This refers to a group of diseases that are related to the bone marrow. They entail the formation of more cells that are required and these cells exhibit abnormality. Platelets are formed in the bone marrow and they are prone to this defect. The myeloproliferative syndromes relate to the formation of cancerous defects that could be malignant neoplasm as other cancers and they could affect the formation of the thrombocytes, (Osterud & Bjorklid, 2006). This will consequently affect the proper blood clotting process leading to coagulopathy, the blood-clotting defect. Myeloproliferative syndromes are classified as polycythemia Vera, essential thrombocytes, myelofibrosis and chronic myelogenous leukaemia. This defect in the formation of the thrombocytes is caused by abnormalities in the myeloid linings of the bone marrow.
Fibrinolysis protects and prevents blood clotting from taking place. The process usually takes place in two phases that are primary fibrinolysis and secondary fibrinolysis. The primary process is a normal body functioning process that is controlled by an enzyme called plasmin where else the secondary fibrinolysis is caused by medicine or medical disorders (Krause, Howells, Buhs, Hernandez, et al, 2005) Coagulopathy are caused by various multifunctional and interrelated factors which include consumption, duration of coagulation and platelets, malfunction of platelets and increased fibrinolysis. Other factors which lead to coagulopathy include affection or compromise of the Coagulopathy system either by infusion of colloids, hypocalcaemia or disseminated intravascular Coagulopathy syndrome, (Betty & Paul 2004).
Pathophysiology of Coagulopathy in trauma haemostasis
Endothelium cell prevents sub-endothelium matrix from coming into contact with circulating platelets by coating the inner wall of blood vessels, (Klingler, Klima, Martinowitz & Fries, 2007). These factors, in turn, convert prothrombin to generate a small amount of thrombin which is very little to convert fibrinogen to fibrin. This jeopardises the clot formation process. Coagulation process thrombin activates thrombin-active fibrinolysis inhibitor which in turn protects the clotting process from being completed and thus left as premature fibrinolysis. The haemostatic system that balances the functioning of various enzymes in the body is regulated by anticoagulant proteins, fibrinolytic processes and inhibitors (Olson et al, 2007). When haemostatics are operating independently, they ensure the formation of fibrins takes place and a large number of them are formed to ensure that bleeding stops and blood clots. It also ensures that subsequent revascularization takes place to maintain and control the flow of blood.
According to Brohi, Singh, Heron and Coats, (2003), the pathogenesis of coagulation in trauma patients are complex and are caused by various factors such as blood loss, hypocalcaemia and hypothermia among others. The tissue damage caused by the injury incurred by the patient leads to activation of the coagulation system which induces the activation of fibrinolysis, (Klingler, Klima, Martinowitz & Fries 2007)
Fibrinolysis activity increases from patients experiencing major and serious injuries, to those with mild to moderate injuries. The activity of fibrinolysis returns to normal after a period of not more than twenty-four hours, (Bernard, Buist & Monteiro, 2003). Patients suffering from trauma, especially elderly patients experience excessive bleeding and reexploration. This is caused by an increase in activations of the haemostatic system, which is particularly related to an increase in postoperative fibrinolysis (Denninger. & De Prost, 2007). Production of thrombin in the blood cells plays a very important part in the development and growth of haemostatic dysfunction, the excessive generating of thrombin leads to consumption of coagulation factors, platelet factors and excessive production of fibrinolysis. Increased fibrinolysis leads to a multiplication of d-dimer. The d-dimer is not usually found in the human blood, they are produced when the coagulation system is activated by the presence of disseminated intravascular coagulation or thrombosis (Denninger & De Prost, 2007).
According to Bernard, Gray and Buist, (2003), Hypothermia induced Coagulopathy is related to temperature changes, they further argue that temperature affects the rate at which coagulation of blood is achieved as temperature affects the rate at which enzymes and hormones responsible for stimulating and enhancing blood coagulation works. Hypothermia affects haemostasis functions by affecting several levels such as platelet functions, coagulation cascade and fibrinolytic system (Bernard, Jones. & Horne, 2009). High temperatures denature and destroy the favourable conditions for enzymes to act as a catalyst in aiding the production of fibrosis. On the other side, when temperatures are extremely low, enzymes are totally unable to function, therefore they become inactive. At this point, the body works to generate heat by increasing the rate of metabolism, when metabolism rate increases, the blood circulation also increases. The increase in blood flow through the veins and capillaries leads to their expansion thus allowing a large amount of blood to flow through and at a very first-rate (Bernard, Jones & Horne, 2009). The expansion of veins and capillaries leads to an increase and uncontrollable bleeding, due to low temperature the clotting process is prolonged and thus bleeding continues. (Bernard, Gray & Buist, 2003).
Betty, and Paul (2004), argue that the effect clotting takes place at a temperature, not beyond 370C. If the temperature goes below the optimum body temperature, the rate of coagulation become very slow and is usually prolonged beyond the normal time required. According to Bernard, Buist and Monteiro, (2003), prothrombin time increases with a decrease in temperature whereas else activated thromboplastin time becomes prolonged. At temperatures of about 330C, the coagulation process is equivalent to 33% factor IX deficiency, despite the presence of all necessary clotting factors (Nolan, Morley & Vanden, 2006).
At a temperature of between 32-350C, the hypothermia is at a mild level, at this point, it leads to platelets dysfunction and impairing of clotting enzymes functions. As the temperature continues to reduce to a range between 28-320C, coagulation processes are further prolonged by the blood clotting process. At this point, oxygen consumption increases, but the rate at which oxygen and blood cells combine to form thrombin is very minimal. At very low temperatures, the activeness of the enzyme is reduced by more than a half. This means that fibroins are produced at a very low rate which, in turn, affects coagulation, (Betty & Paul 2004).
According to Charbit, Mandelbrot, Samain, Baron, Haddaoui, Keita, Sutherland and Corbett, (2005), if temperature reduces further to a point below 280C, the coagulation process never takes place as enzymes are totally denatured by the fall in temperature levels leading to enzymes becoming inactive. In other words, it means that fibroins will not be produced, as enzymes cannot be active within this temperature. At a point where the temperature is below 280C, the tissue oxygen consumption becomes very limited and leads to the production of insufficient heat to raise temperature to the optimum point, (Nolan, Morley, & Vanden, 2006).
Enzyme inhibitors theories
Enzyme inhibitors are factors that alter the actions of the catalyst of an enzyme thus slowing down or stopping the catalyst from functioning. A number of factors affect the rate at which enzymes work in forming blood clots (Charbit, Mandelbrot, Samain, Baron, Haddaoui, Keita, Sutherland and Corbett, 2005). These inhibitors include nonspecific, reversible, irreversible, competitive and non-competitive. Poisons and drugs also act as enzyme inhibitors. Nonspecific inhibitors prevent all enzymes from performing any functions by either physically or chemically denaturing the protein portion of the enzyme thereby lending it inactive. When an enzyme is fully destroyed, the fibrinolysis is not generated and thus blood clotting will not take place at a speculated time but will be delayed and take place at a very low pace. When the temperature is not conducive for an enzyme to play its role as a catalyst, the blood clotting is seriously affected. According to Oku, Sterz and Safar, (2009), temperatures determine the rate at which an enzyme functions at optimum level.
Bernard, S., A. & Buist, M. (2009). Induced hypothermia in critical care medicine: a review. Critical Care Medical, 31(7) Pp. 2041-2051.
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