Clotx Essay

CLABSI’s, or Central Line Associated Bloodstream Infections, are a worldwide problem of bloodstream infections from the unsterile insertion or unclean maintenance of a central line catheter, which are inserted in large veins and are in place for weeks or months (CDC, n.d.). CLABSIs have a high morbidity and mortality rate, increases cost of medical treatment and extends the length of hospitalization (Poderman & Girbes, 2002). Implementing evidence based practices have significantly reduced these CLABSI rates (Latif et al., 2015). CLABSI prevention research shows overlap in these five areas of evidence-based prevention: appropriate hand hygiene, skin preparation, use of full barrier preparations, avoidance of femoral site for central line

Identifying what factors contribute to occlusion are background questions (Melnyk & Fineout-Overholt, 2015) that should be addressed to ensure the foreground question is appropriately answered. Medication administration, fibrin sheath formation, duration, and frequency of use can each contribute to clot formation (Gabriel, 2011). If a patient is scheduled to receive a specific medication over a duration of time, it is imperative that the central venous catheter is patent and available for continuous use. Encouraging patient compliance will assist with ensuring that duration and catheter access doesn’t increase the risk of clot

The Oxyglobin and Hemopure substitutes developed by Biopure have an advantage over blood transfusions in many areas including blood type matching, universality in terms of donating, such as O+ blood recipients. The blood substitutes also had a much longer storage life of 2 years as opposed to the 6-week storage life of transfused blood. Furthermore, with the rise of diseases such as AIDS and increasing public concern about the same, blood substitutes also helped mitigate that risk. Baxter International and Northfield Laboratories-products sourced their blood substitutes from human blood whereas, Biopure sourced it from animal blood, cattle in particular. This put them in a better position than their competitors. Also Biopure’s Hemopure and Oxyglobin did not require refrigeration unlike its competitor’s products.

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).

Hemostasis is the process whereby blood coagulates at the site of an injury to a blood vessel. Cellular components involved in hemostasis include platelets, endothelial cells of blood vessels, tissue factor-bearing cells, and coagulation factors (Davoren & Wang, 2014). Coagulation factors are specialized plasma proteins that circulate in the bloodstream in inactive forms. Most coagulation factors are activated by enzymes that catalyze their conversion to active forms. The active forms then contribute to hemostasis. Factors VIII (FVIII) and IX (FIX) are the factors involved in the most common forms of hemophilia. The coagulation cascade has many steps and reciprocal interactions; however, FVIII and FIX are most involved with the following steps:

Tissue plasminogen activator is a fibrinolytic drug which is used to treat thromboembolic disorders, such as ischaemic strokes. These agents initiate secondary fibrinolysis to occur; altering the haemostatic capability. The primary purpose of this agent is to clear occluded blood vessels within the systemic circulation (Bryant & Knights 2011, pp.534-536).

Exclusion criteria for the study included: Patient refusal to consent (absolute), infection in the patients back near the proposed site of the injection, coagulation disorder :-( defined as PT: > 18 sec, PTT: >40 sec, I.N.R: > 1.5, clotting time: >8 min, platelet disorder: platelet count: < 100.000, bleeding time: >4 min, HELLP Syndrome: - (defined as Hemolysis, Elevated Liver enzymes, Low Platelet count), receiving any anticoagulant drugs, preexisting neurological disease or psychic patients, history of cardiac and respiratory system failure, known allergy to local anesthetics drugs, coexisting renal disease and eclamptic patients.

Heart disease is the number one cause of death in the United States per the Center for Disease Control (Heart Disease Facts). All students, regardless of gender and ethnicity, should be taught the importance of cardiovascular health in biology class so they can improve their wellbeing and identify risk factors for themselves and family members to prevent complications or death from heart disease. As new technologies emerge, in the form of health screening, medication and surgical procedures, doctors can better manage and detect heart disease. Also, called cardiovascular disease, heart disease is defined as narrowed or blocked blood vessels or arteries that causes reduced blood flow, chest pain (angina), or heart attack. A heart attack is when

In the face of hemorrhagic and ischemic shock with endothelial damage, fibrinogen levels fall dramatically. Decreased fibrinogen levels directly alter the body’s ability to form the fine meshwork needed to achieve hemostasis. Normally, thrombin breaks down fibrinogen into fibrin to assist in providing the scaffolding for clotting. When severe tissue injury occurs, the lack of fibrin cannot form the mesh needed to assist in clot formation. The 2010 RCT CRASH-2 study displays the strongest evidence proving that administering tranexamic acid(TXA) to severely shocked trauma patients(MAP <75 mmHg) reduces the amounts of death from bleeding in this population from 18.4% to 14.9% (Napolitano, Cohen, Cotton, Schrieber, & Moore, 2013). Simply put, TXA prevents plasminogen’s conversion to plasmin. The inactivated plasminogen will then allow the clot to become more secure. Because of plasmin’s inherent ability to degrade fibrinogen, the patient’s d-dimer which measures fibrin degradation products, the patient with ATC will have elevated d-dimer levels. Low fibrinogen levels in a patient with ATC warrants cryoprecipitate infusion and has been associated with increased survival outcomes (Rourke, 2012).

Pulmonary embolism, synonymous with deep vein thrombosis; are important and is a growing public health problem. Both contribute to the 300,000-600,000 individuals affected by this each year in the US alone. This condition does not discriminate against age, gender, or race and occurs across all boards causing morbidity and mortality. When misdiagnosed, unrecognized, or untreated, PE can cause death quickly; within just an hour. It’s fatal in up to 26% of cases (Andrews, 2010). However, prompt treatment greatly reduces the risk of death. Taking the necessary preventative measures to prevent blood clots is the key to protecting one’s self of these conditions.

Efficient inhibition of the fibrin deposition and thrombus formation by plasma protease FXIIa-neutralizing antibody, 3F7, by binding specifically to the enzymatic pocket of FXIIa in an extracorporeal membrane oxygenation (ECMO) system similar to heparin but without treatment associated increase in hemorrhage signifies thromboprotective properties of 3F7. Further, inhibition of the thrombus formation without impairing the hemostasis indicates FXII as a potential target for prevention of atherothrombosis. The use of ECMO simulating the clinical settings signifies the meaningful importance of this study to use in clinics. However, the prevention of the contact-induced FXIIa formation, thrombus formation in mice and rabbits and coagulation in-vitro with 3F7 has also been documented [59,60,61] (Figure 2). FXII activation is also mediated by inorganic polymer polyphosphate (polyP), which is stored in platelets and secreted on platelet activation [36]. Reduced fibrin accumulation and attenuated thrombus formation without increased risk

Despite considerable advances in surgical treatment, the ruptured human abdominal aortic aneurysm (AAA) is still associated with a mortality rate of 65–85% [1, 2] . A diameter is currently the only reliable determinant of the imminent rupture of an AAA and patients exceeding 5.5 cm generally undergo surgical or endovascular intervention [2, 3] . However, the outcome of rupture is poor with less than half of the patients being delivered to the hospital alive [1, 4] . It is well known that inflammation and proteolytic degradation markedly contributes to the formation and rupture of an AAA [5, 6] . During inflammation, the aortic wall is weakened by loss of smooth muscle cells (SMCs) and destruction of the extracellular

Disseminated intravascular coagulation (DIC) is a systemic process, characterized by widespread activation of blood coagulation. This leads to microvascular thrombi in organs and subsequent exhaustion of coagulation products, which then leads to severe systemic bleeding (Levi, 2015). DIC can exist in both acute and chronic forms. Acute DIC develops when the body is suddenly exposed to procoagulants (tissue factor (TF). This then leads to intravascular coagulation. In acute DIC, compensatory hemostatic mechanisms become exhausted with the systemic coagulation, which eventually leads to severe hemorrhage. In chronic DIC, the compensatory hemostatic mechanisms are not exhausted due to smaller amounts of chronic TF, so severe intravascular coagulation or bleeding does not occur. In chronic DIC thrombosis usually predominates over bleeding, and many patients can be even asymptomatic (Leung, 2015). DIC is estimated to occur in 1% of hospitalized patients. DIC is not a specific illness, but rather a complication of an underlying condition or disease (Levi, 2015). Identifying DIC and treating the underlying cause promptly, is vital to treating DIC.

Hypertension is one of the major risk factors for the development of cardiovascular diseases including stroke and may also have a role in the development of vascular cognitive impairment and vascular dementia [1, 2]. Angiotensin I-converting enzyme (EC 3.4.15.1; ACE) plays an important role in the rennin-angiotensin system and it is a carboxyl-terminal dipeptidyl exopeptidase that catalyzes the conversion of angiotensin I to angiotensin II [3-6]. ACE converts an inactive form of decapeptide, angiotensin I, to a potent vasoconstrictor, octapeptide, angiotensin II, in addition; since the ACE is a multifunctional enzyme it also catalyzes the degradation of bradykinin, which is known as a vasodilator [4, 7]. Therefore, inhibition of ACE

In the normal extrinsic blood coagulation cascade, tissue injury causes expression of tissue factor. Tissue injury also causes exposure of the subendothelial components, which includes Von Willebrand Factor (vWF) and collagen. vWF holds platelets together and is a carrier protein for fVIII in plasma. Tissue factor binds to factor VIIa (fVIIa) to form a complex that cleaves fX into fXa to activate it. Prothrombin is then converted into thrombin by the promthrombinase complex formed from fXa and fVa. Clotting requires both calcium and a phospholipid surface. The intrinsic coagulation cascade and coagulation factors that’re activated increase the amount of clotting there is.