Introduction
Deep vein thrombosis (DVT) is frequently seen in patients seeking healthcare services in hospitals. DVT can lead to severe morbidity and enhance mortality in the general populace. The incidence of DVT in the United States of America is estimated at about one in every thousand person years. However, reliable incidence data is not truly available as autopsy results often show the presence of DVT, even when there is no clinical suspicion of DVT. So reliance on hospital discharge diagnosis or on death certification hardly provides a true indication of the exact incidence of DVT in any population (Rodriguez & Schwartz, 2003). Such a scenario may have arisen from the impression that superior vein thrombosis (SVT) due to its benign course, often being ignored as a possible sign of DVT. According to the American Public Health Association 2004, DVT and the complications that result from DVT us responsible for as many as 200,000 deaths in the United States of America every year, and many of these deaths could have been prevented. It is the frequent exposure to DVT in the clinical environments die to high incidence of DVT and the high morbidity and mortality associated with DVT that has evoked interest in DVT and the reason for this paper.
Predisposition to DVT
Since the beginning of the twentieth century three factors were considered as being responsible for the predisposition of an individual for DVT. These three factors were a high state of coagulability, trauma to the vascular intima, and venous stasis. Evidence from over these hundred years suggests that such a consideration of the predisposition of an individual to DVT was true, as the currently held predisposition factors show. The current understanding of CVT shows that several factors influence the predisposition to DVT, which are a combination of genetic risk factors and acquired conditions. Estimates suggest that genetic causes are responsible for 25% of the cases of DVT, and where there is a family history DVT this percentage increases to 63% clearly indicating genetic factor responsibility. The elevated levels of factor VIII5 and high plasma homocysteine levels are important among the factors considered to be responsible for DVT. Among the acquired predisposition factors for DVT stasis is the most frequently encountered precipitating factor. Enhanced age, obesity and restriction to movement, smoking and prolonged travel aggravate any of the acquired predisposition factors (Rodriguez & Schwartz, 2003).
Surgical interventions are found to be responsible for the final precipitating factor of vascular injury leading to DVT. There is general acceptance that orthopedic surgery has a very high risk potential for postoperative venous thromboembolism. The high potential or venous thromboembolism (VTE) has many factors that contribute to it. Injury to the blood vessels is one factor. The second factor is venous stasis of the legs and arms. The third factor is advance in age and the reduction in mobility (Rodriguez & Schwartz, 2003).
Pathophysiology of DVT
In the opinion of James, Ortel, and Tapson 2008, p.6 the pathophysiology of DVT can be defined as “the formation of a blood clot in one of the deep veins of the body, usually a vein in the muscle of one of the legs” (James, Ortel & Tapson, 2008).
There are two forms of DVT namely non-occlusive thrombosis and occlusive thrombosis. In non-occlusive thrombosis blood flow in the vein is not fully blocked, whereas in the case of occlusive thrombosis the blood flow in the vein is fully blocked. Evidence from studies are demonstrative of the figures that in 77% of the cases DVT occurred in one leg, while in 12% of the cases DVT occurred in both legs, and in about 11% of the cases the occurrence of DVT was in the arms. This shows that the occurrence of DVT is essentially confined to the legs and arms with rare episodes of DVT in other parts of the body like brain, neck, liver, pelvis, and inferior vena cava (James, Ortel & Tapson, 2008).
The hypercoagability state associated with DVT is the consequence of the disruption of the normal balance that exists in relation to the procoagulant system and the anticoagulant system in the human body. In normal body function the anticoagulant system attempt is to confine the beneficial thrombotic effect to the site of injury and thereby prevent its propagation. The factors associated with this anticoagulant system are tithrombin III, Protein C, and Protein S. Protein starts acting as a response to the activation of enzyme APC, which performs the function of a natural anticoagulant through the inactivation of the procoagulant factors Va and VIIIa, when protein S is present. Antithrombin III has the action of directly of directly inhibiting thrombin. Mutation of the Factor V Leiden can inhibit the normal functioning of the anticoagulant system of the human body. In addition the normal functioning of the anticoagulant system of the human body can be negatively affected by deficiencies in the availability of Protein C, Protein S, and antithrombin. The high plasma levels of prothrombin 20210A and factor VIII have the action of accelerating the working of the procoagulant system and enhancing the risk for DVT. Research in molecular genetics is trying to uncover other prothrombotic mutations that are responsible for enhanced risk for DVT (Rodriguez & Schwartz, 2003).
Evidence from studies has clearly demonstrated that normally DVT develops in the veins of the calf muscles of the legs and then progress proximally. Though there is less clarity on the development of DVT in pregnant women, there are indications that proximal deep vein thromboses, with particular emphasis on iliofemoral are frequently seen in pregnant women and the anatomic distribution of these thromboses vary significantly from women who are not pregnant, suggesting that it would be useful to examine the iliofemoral venous system, when there is suspicion of DVT in pregnant women (Wee-Shian et al, 2010). Variance of the development of DVT in pregnant women from that of non-pregnant women receives support from Risto 2010, who further suggests that in pregnant women there is no usual route for the development of DVT. In pregnant women the development of thrombosis and its propagation are seen to be different on the basis of the various risk factors pertinent to the case of each pregnant woman the thrombosis and propagation can be different based on the risk factors of thrombophilic status. These risk factors include the affect that the growing uterus has on the possibility of venous stasis of the lower extremities and the requirement for immobilization during pregnancy (Risto, 2010).
Complications with DVT
The blood clot responsible for DVT can break away from the site of DVT and move along to other parts of the body causing serious complications in other parts of the body. This clot can travel along the blood vessels and makes its presence felt in the lung artery as pulmonary embolism (PE). PE is a major complication with DVT that can have serious consequences including death of the patient. PE remains the most significant complication that leads to death in patients with DVT. Postthrombotic syndrome (PS) is a more common complication associated with DVT, with as many as two thirds of patients with DVT landing up with PS. The continuing presence of a blood clot for long periods of time in the veins of the lower extremities can damage the valves of the veins. As a consequence blood can flow back the blood due to the action of gravity. Reflux in the vein can result in blood pooling in the leg, which can cause pain in the leg, swelling of the leg, darkened skin color, skin ulcers, varicose veins, recurrent deep vein thrombosis, PE. The more rare risks associated with DVT include blood clot in the kidney or renal vein thrombosis, thrombosis in the heart that can cause heart attacks, and blood clot in the brain and the resultant stroke (Bryg, 2009).
Treating DVT
There are four objectives associated with the treatment of DVT. These objectives are prevention of mortality from pulmonary embolism; alleviation of the common symptoms of pain and swelling associated with DVT; preventing morbidity of the patient as a result of recurrent DVT or PE; and preventing post-thrombotic syndrome in the patient and making the post-thrombotic symptoms as minimal as possible (Raskob, 2009).
In most patients these objectives are met by the pharmacological intervention of anti-coagulant therapy consisting of heparin as initial treatment and long term treatment extending to six months (Raskob, 2009). Initial treatment using oral anticoagulant therapy is insufficient. The recommended start to the treatment of DVT is the appropriate doses of unfractionated heparin or LMW heparin. LMW heparin is easy to administer and so remains the choice in anticoagulant therapy in clinical or home settings. LMW heparin is effective as lesser mortality, reduction in major hemorrhage and recurrence has been reported through its use. Another useful alternate pharmacological agent is fondaparinux, which is effective and also provides the advantage of absence of heparin induced thrombocytopenia (Dimitrios & Wells, 2006).
Non-pharmacological interventions can be used to reduce the swelling and pain associated with DVT. The non-pharmacological intervention involves ambulance along with compression of the leg in medically patients with DVT. Evidence from randomised controlled studies has shown that the combination of compression and ambulation reduces thrombus progression, pain, and swelling (Dimitrios & Wells, 2006).
Rationale for a Health Care Team in DVT
The management of DVT involves different disciplines involved in providing the required service. No single discipline is capable of providing all the DVT management services required. The management involves different treatment modalities that consist of pharmacological treatments extending to surgical interventions. The complications that can arise from DVT could implicate several vital organs of the body requiring specialist attention. Non-pharmacological interventions are involved once the patient has been stabilised. These factors contribute to the requirement of a health care team consisting of medical, surgical and specialist clinicians, pharmacists, physiotherapists and last but nit the least nursing professionals (Robinson, 2006).
Role of the Nursing Professional in the Healthcare Team
The management of DVT involves procedures, diagnostic tests, therapies, treatments, and medications. The nursing professional will have to plan and schedule all these activities involving the patient. This would call for the development of organizing skills and resourcefulness on the part of the nursing professional. Several procedures, treatments and therapies are involved and there is the need for evaluation of the interventions in meeting the outcome objectives for the concerned patient. The nursing professional plays a key role in this evaluation and also in patient satisfaction. These activities need to be coordinated and monitored, which requires good verbal and written communication skills. Ensuring that appropriate communication to the other members of the team is maintained in keeping with the quality standards in meeting patient care needs is a part of the role of the nurse. Finally monitoring all these activities requires maintaining records in a user friendly manner that can be accessed and seen by the other members of the team (Daniels, 2004).
Conclusion
There is a high incidence of DVT in the United States of America. Complications arising from DVT are the cause of many deaths. Many of these complications of DVT can be prevented. These factors make it necessary for healthcare professionals to be aware of the risks factors of DVT, its development in the body, the progress of DVT in the human body, the complications that arise from it, and the treatment and prevention modalities. The care needs of patients with DVT are such that it cannot be managed by any single discipline that provides health care needs. As a result care needs of a patient with DVT are provided by a healthcare team. The nursing professional plays a pivotal role in ensuring the quality of care provided by the healthcare team.
Literary References
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James, A. H., Ortel, T. L. & Tapson, V. F. (2008). 100 Questions &Answers About Deep Vein Thrombosis and Pulmonary Embolism. Sudbury, MA: Jones and Bartlett Publishers.
Raskob, G. (2004). Initial and Long-Term Treatment of Deep Vein Thrombosis. In Edwin, J. R. Van Beek, Harry R. Buller & Oudkerk, Mathijs (Eds.) Deep Vein Thrombosis and Pulmonary Embolism (pp. 475-486), Oxford: John Wiley & Sons.
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Wee-Shian, C. (2010).. Anatomic distribution of deep vein thrombosis in pregnancy. CMAJ: Canadian Medical Association Journal, 657(4), 182-187.