Sample Nursing Research Paper on Maintaining an adequate fluid balance to prevent platelet aggregation toward thrombi formation

Maintaining an adequate fluid balance to prevent platelet aggregation toward thrombi formation

Introduction

The process of hemostasis is essential where there is need to control excessive hemorrhage. However, this process can also lead to adverse clinical effects if not controllable where occlusion occurs in blood vessels. According to a research carried out by Freedman (2005), occlusive thrombosis is a leading cause of mortality and morbidity and thus requires measures for effective management. The key objective of thrombosis management in this case would be to maintain a balance between the occlusive and the non-occlusive thrombus formation processes. While the non-occlusive thrombosis is essential in hemorrhage prevention, the occlusive one is more undesirable in the clinical set up. When occlusive thrombosis occurs in arterial and venous blood circulation, the effect is more potentially detrimental. While giving recommendations for the management of cardiovascular diseases, the Registered Nurses Association of Ontario suggests prevention of thrombosis in the venous system (2013).

Thrombosis occurs as a function of several factors. In the entire process, the role played by the activation of platelets is an essential role, yet complex to understand. The platelet activation process itself is influenced by factors such as biochemical and mechanical processes that are subject to myriad plasma and cellular derived mediators. In entirety, the platelet activation process results in the aggregation of platelets which in most cases occurs close to vessel walls. It is this aggregation that ultimately leads to the thrombosis process which may be occlusive or non-occlusive. The prevention of occlusive process therefore depends to a large extent on the ability to prevent platelet aggregation near the vessel walls.

The present literature review aims at finding ways through which platelet aggregation that leads to thrombosis can be prevented particularly through fluid balance. As is reported by Williams and Wilkins (2004) maintaining an adequate fluid balance can help to prevent platelet aggregation through maintenance of sufficient blood pressure in the vessels. The review therefore aims at determining ways in which this can be achieved. The question to be answered is thus “how is fluid balance maintained in the body to prevent platelet aggregation towards thrombosis?”

Problem concern to nursing

The issue of thrombosis is of concern to nursing in various contexts. While hemostasis may be essential where there is need to prevent excessive bleeding in patients, it may also pose a challenge where it occurs in unprecedented extents. Operative procedures involving large amounts of blood loss are especially targeted through procedures for both hemorrhage and thrombosis prevention. This is because not only does thrombosis make bleeding management a problem, but it also results increased chances of mortality. In a report on the facts about cardio vascular diseases, the World Health organization reports that preventing thrombosis that results from platelet aggregation can be an important step in preventing the fatality of CVDs (2013). However, this cannot be achieved through dependence on genetic factors alone.

From the work done by Freedman (2005), it was confirmed through a systematic review that occlusive thrombosis results in various clinical effects such as thrombotic vascular events and myocardial infarctions. The implication of this is that while thrombosis itself may not be seen as potentially dangerous, the effects may result in long term clinical needs which may prove difficult to manage. The management of platelet aggregation processes is thus necessary particularly due to the reason that platelets form the highest concentration of blood cells. At the same time, platelets themselves prove challenging to manage in that although they have similarities to other cells to a large extent i.e. in they have biological mechanisms that are similar to other cells, they lack nucleus and are therefore unable to adapt to changes in the biological environment.

The differences between platelets and other cells make it easier for them to react adversely to changing biological environments through effects such as aggregation. To prevent such effects, the biological environments can thus be changed to cater for the reactions of the platelets particularly where blood changes have occurred. In the clinical set up, this is mainly achieved through maintenance of adequate fluid balances by fluid resuscitation using either crystalline or colloid fluid make ups.

Literature Review Body

Various studies have been carried out to determine the mechanical and biochemical factors that initiate and advance platelet aggregation towards thrombosis. While most of the studies carried out do not effectively describe the method of maintaining adequate fluid balance to prevent platelet aggregation, one important point of agreement across various studies is the role played by fluid balance on the aspect of preventing aggregation of platelets (Freedman, 2005; Anand et al., 2003). Anand et al describe the process leading to thrombus formation as involving platelet activation followed by adhesion to vessel walls and finally aggregation. This implies that the availability of stimuli for platelet activation initiates the process of aggregation and eventual thrombosis.

While biochemical and hemodynamic factors influence the degree of aggregation towards thrombosis, the key influence is accorded to flow conditions around the area of aggregation. At points of high shear stress, there is low potential for thrombotic eventualities while where the shear stress is high; the formation of thrombus is inevitable (Hathcock, 2006). From Williams and Wilkins suggest that it is the role of blood itself to provide adequate fluid amounts as well as to maintain a balance of salts and proteins for the prevention of excessive blood loss as well as prevention of pathologic hemostasis (2004). This means that as long as blood volumes are low, the amount of fluid in the body will remain low. Similarly, when the balance of proteins and salts in the blood is low, the effect is adverse. To prevent this, it is essential to always maintain adequate fluid amounts through provision of resuscitative fluids where necessary.

The need for maintaining adequate fluid balance is also discussed by Spahn et al (2013) in a report based on the review of various RCTs. In their report, Spahn et al discuss the need for constant monitoring of factors such as platelet counts, prothrombin time and fibrinogen which are key actors in the thrombosis process. According to this report, maintenance of adequate fluid volumes following the measurement of such factors in post-operative observation is an essential way of preventing coagulopathy in trauma patients. Furthermore, the need for fluid transfusion depends on the findings from the measurements since there are cases where platelet transfusion may be needed i.e. when there are higher chances of hemorrhage. On the other hand, fibrinogen transfusion may be necessary when the rate of thrombosis is high (Spahn et al., 2013). The loss of blood during operative procedures results in most cases to a reduction of blood volumes and subsequently the loss of platelet count. However, although the fluid volumes may reduce where there is excessive bleeding, the reduction in the amount of thrombotic agents is generally low unless more than 2 pints of blood are lost (Spahn et al., 2013). This means that the higher the level of blood loss, the greater the concentration of the remaining thrombotic agents per unit volume of blood. Platelet concentration also increases with reduction in blood volumes and thus makes it necessary to ensure that platelet counts per unit volume are adequate for the prevention of platelet aggregation (Harris & Kuppurao, 2012).

The effect of massive loss of fluid volumes is best described by Anand et al who assert that clot formation due to platelet aggregation occurs when there is an imbalance between the blood components in favor of pro-thrombotic factors. In addition to this, the authors claim that there is a threshold amount of stimulus beyond which platelet activation and subsequent aggregation occurs. However, this threshold is more easily reached where the amount of fluid volumes is low and the level of shear stress is reduced. As a way of expounding on the effects of reduced fluid volumes on the activation and aggregation of platelets, Anand et al elaborate how blood operates like a shear thinning fluid, a property that makes it essential to prevent platelet aggregation through maintenance of adequate fluid balance. However, the effectiveness of the preventive process depends not only on the ability to maintain adequate fluid balance but also on several other factors which are linked to the hemodynamic conditions of the body. Factors such as availability of catalytic binding sites, conditions of local blood flow, concentration of coagulation factors and platelets and the concentration of divalent ions such as Ca2+ all influence the aggregation properties of platelets during bleeding (Anand et al., 1998).

In various studies, the focus on resuscitation through fluid addition has been limited to the role played by colloid and crystalline fluids in the blood. According to Anand et al, the hemostasis can be either safe in that it results in the prevention of excessive blood loss or may be pathological. However, the pathological aspect only comes about when there is hypo or hyper functioning of any of the blood components related to fluid balance. This can be explained from the point of view presented by Hathcock in that the concentration of enzymes and substrates also affects the process of thrombosis. Although this is not clearly articulated, it can be deduced that pro-thrombotic factors operate depending on the availability of effective shear stress as well as on their ability to be sustained by the available substrates and that the reaction only goes on as long as there is sufficient catalysis. The process can be made more comprehensible through an explanation of the blood flow characteristics as described by Anand et al.

According to Hathcock (2006) factors such as the presence of red blood cells, platelets and leukocytes as well as sufficient shear stress result in the formation of stable aggregates between each other as well as within themselves. The shear stress below which pathological aggregates form is described by Anand et al as the threshold shear stress and can be avoided through maintenance of sufficient fluid pressure.  Hathcock asserts that the aggregates formed by platelets, red blood cells and leukocytes can alter the biochemical make- up of the aggregates themselves as well as that of the cell walls. One of the key effects of this would be an increase in blood viscosity, resulting in greater potential for thrombosis. Apart from this, the aggregation of these components also influences the biochemical make- up of the thrombi that results due to aggregation and the reaction pathways that eventually lead to thrombi formation. The influence of aggregation on both aspects is more adverse than essential towards the management of thrombi formation. Hathcock claims that during high flow velocities, the diffusive motion of cells and proteins in the region of thrombosis is low hence the rate of thrombosis are effectively reduced. High fluid velocities are only maintained through adequate fluid pressure.

From the description by Anand et al (2003), platelets are usually undamaged in the blood. However, during aggregation and thrombosis, the activation of platelets can be described as a more or less damaging effect on them. This means that as long as there is aggregation of platelets, it is impossible to say that the platelets are undamaged. Activation however only occurs once a threshold activation number has been reached. According to authors such as Hathcock (2006), Anand et al (2003) and the World Health Organization (2013), it is essential to maintain adequate fluid volumes to prevent aggregation by maintaining a sufficient fluid pressure in the body. This is in line with the recommendations made by Hathcock, to increase fluid shear rates and raise fluid velocity through the maintenance of sufficient fluid volumes in the body.

While various authors recommend resuscitative fluid administration to manage the volumes of fluid flow and subsequent flow pressure, there are also claims that colloid and crystalloid fluid make-ups have not been confirmed effective for the prevention of platelet aggregation towards thrombus formation (Hathcock, 2006; Anand et al., 2003). Moreover, Spahn et al also explain that in cases where there has been massive blood loss and coagulopathy, aggressive administration of make-up fluids may not be effective towards the achievement of the desired intervention outcomes. This is further explained through the assertion that a high volumetric rate of resuscitation fluid administration creates very high pressures at the wounds which result in the dislodgment of clots and increased bleeding. It can thus result in hemorrhage rather than restoration of lost blood pressure. In addressing this issue, the authors recommend the administration of resuscitative fluids at low rates referred to as permissive hypotension (Spahn et al., 2012).  In this case, the maintenance of adequate vascular volumes is mandatory not only to prevent platelet aggregation but also to manage body rehydration where there is massive blood loss. Spahn et al assert that despite the ineffectiveness for improved outcome in hemorrhage patients, administration of resuscitative fluids can be the determinant of life where coagulopathy is occurring at high rates. This is through the maintenance of sufficient blood pressure and volumes, rehydration as well as creation of sufficient shear stress for the dislodgment of aggregated platelets.

While the findings from various studies show that fluid resuscitation can aid in aggregation inhibition which eventually protects the patient from thrombosis, the authors also clearly communicate their concerns about the possibility of increased bleeding as a result of thrombosis prevention. The key objective is thus recommended to maintain a balance between the increased bleeding potential and the prevention of platelet aggregation. Achieving this is however a feat that is difficult to reach since this requires the maintenance of an exact amount of blood in which the body is consistently under sufficient flow pressure.

Conclusion

The literature review carried out provides an overview of the various recommendations provided by different authors on how to maintain an adequate fluid balance towards prevention of platelet aggregation. In answering the research question the literature review has done well although to a limited extent. The suggestions of authors such as Hathcock on maintaining adequate fluid balance still play an important role in modern day nursing towards the accomplishment of thrombosis prevention in patients. It is important to note the events leading to platelet aggregation and subsequent thrombosis as well as the factors that contribute to the initiation and advancement of the process. This can only be achieved through reading materials that provide such information. For instance, Anand et al describe the blood flow dynamics effectively, and link the flow mechanisms directly to the subject of platelet aggregation. In their description, blood is characterized as a shear thinning fluid whose flow is influenced by several factors, key of which is the volume of blood.

From the studies highlighted, it is clear that maintenance of adequate fluid balance helps to prevent thrombosis by preventing aggregation of platelets. The effect of increased blood volumes is placed on the link between blood volume increments and the flow pressure in the vessels. This means that the only way in which medics can prevent platelet aggregation towards thrombosis is through maintenance of adequate fluid balance since other factors such as substrate and enzyme concentrations, concentration of pro-thrombic factors and the concentration of leukocytes, red blood cells and platelets are beyond the control of the clinician. In effect, increasing blood flow velocity increases shear stress in the area of the thrombosis and thus disburses the already formed thrombi while also raising the activation number of the system far beyond the threshold value. This eventually leads to prevention of platelet aggregation. The only way in which adequate fluid balance can be maintained is through provision of adequate amount of resuscitative fluid which can be either crystalloid or colloid. Either way, it has been confirmed that fluids with high concentrations of Ca2+ are more likely to achieve the desired prevention of platelet aggregation.

The literature review has been effective in providing informative information particularly regarding the maintenance of adequate fluid balance for prevention of platelet aggregation towards thrombosis. However, there are various challenges that arose during its compilation. First, studies focusing on the aspect of fluid balance with respect to prevention of platelet aggregation. The available pieces of literature address platelet aggregation and fluid balance independently, making it difficult to create a connection between the two. Moreover, most of the available works on same are from long ago despite being relevant to date. It is thus difficult to predict whether the available information is still exactly applicable as it is or if there is new information or modifications to practice that have arisen in the recent years.

It can therefore be concluded that despite the effectiveness of the literature review in answering the objective question, it is still limited in terms of scope and practical application. Greater evidence that goes beyond description of the applications of fluid balance to the prevention of platelet aggregation is thus necessary. This can only be achieved through greater learning opportunities that are based in a clinical set up.

Potential Research Questions

The literature review has clearly shown the importance of maintaining an adequate fluid balance towards the prevention of platelet aggregation. However, there still remains an important opportunity for future research to be expanded. In order to achieve this effectively and to find practical applications of the process of maintaining adequate fluid balance, it is necessary to follow the following recommendations. First, future research should be aimed at not only explaining the blood flow characteristics and finding the link between blood flow and platelet aggregation, but also explaining how various characteristics of blood influence the aggregation of platelets. What this means is that apart from the explanation of the shear characteristics and their influence on aggregate formation, studies should also focus on how characteristics such as platelet counts, substrate concentrations, and local flow conditions can be used to prevent platelet aggregation.

Secondly, the present literature review has brought out the need for advanced research through an indication that there is currently limited information regarding the subject of this research. This offers future studies an important point of entry into research through suggestion of an unsaturated topic of research. It purposes to show potential researchers that time invested in the present research subject is not wasted as it will contribute immensely to the academia and to the clinical set up as well. The question is still however how to effectively manage fluid volumes and compositions towards an effective end.

In conclusion, while researchers aim at finding out how to maintain adequate fluid balance for the prevention of platelet aggregation towards thrombosis, it is critical that they also address the need for maintaining a balance between the potential for excessive blood loss and the prevention of thrombosis. How this can be achieved through fluid resuscitation is still a challenge.

References

Anand, M., Rajagopal, K. and Rajagopal, K.R. (2003). ‘A Model Incorporating some of the Mechanical and Biochemical Factors Underlying Clot Formation and Dissolution in Flowing Blood.’ Journal of Theoretical Medicine, 5, 3-4, 183- 218.

Freedman, J. (2005). ‘Molecular Regulation of Platelet Dependent Thrombosis.’ Circulation, 112, 2725 – 2734.

Harris, P. and Kuppurao, L. (2012). ‘Ventricular Assist Devices.’ Continuing Education in Anesthesia, Critical Care and Pain, 12,3, 145-151.

Hathcock, J.J. (2006). ‘Flow Effects on Coagulation and Thrombosis.’ Arteriosclerosis, Thrombosis and Vascular Biology, 26, 1729 – 1737.

Registered Nurses Association of Ontario (2013). Assessment and Management of Pain 3rd Ed. Toronto, ON: Registered Nurses Association of Ontario.

Spahn, D., Bouillon, B., Cerny, V., Coats, T., Duranteau, J., Filipescu, D. et al. (2013). ‘Management of Bleeding and Coagulopathy following Major Trauma: An Updated European Guideline.’ Critical Care, 17, R76.

Williams, L. and Wilkins, L. (2004). Straight As in Nursing Pharmacology. Wolters Kluwer Publications

World Health Organization (2013). ‘Cardiovascular Diseases.’ WHO.