Portal Vein Thrombosis Case Study

One of these symptoms is jaundice, which is characterized by yellowish skin and eyes because of an inability of the liver to remove bilirubin from the blood. Patient with cirrhosis also suffering from itching, due to deposited bile's products in the skin. This patient also suffers from accumulation of fluid in legs that is called edema. As a result of the blockage of blood flow via the liver, fluid accumulation in abdomen which is worsen by the decrease in protein production. Other symptoms include fatigue, weakness, loss of appetite, weight loss and nausea. As the disease progress, complications may develop ,such as varices that happens with cirrhosis patient when the blood flow through the liver slows, so the blood from intestine go back to the vessels of the stomach and esophagus, these vessels are not meant to carry this much of blood so they dilate (varices), with increasing

* Esophageal Varices Bleeding: scarring of liver causes blood flow through the liver to decrease. With the decrease in liver blood flow, more blood pumps through veins causing them to balloon outward. The increased amount of blood in the veins results in a vein bursting and leads to bleeding. This condition is secondary to portal hypertension because of the alternate routes the blood takes due to the scarred liver, causing the veins to work harder and accumulate more blood within a certain span of time, not being able to drain in a timely matter.

This year, an estimate of 53,070 adults, have been or will be diagnosed with pancreatic cancer. (27,670 men and 25,400 women). Pancreatic cancer is the ninth most common cancer in women. Pancreatic cancer should have the most attention because doctors still don’t know how to diagnose this type of cancer yet. The main problem is cost-effective screening tests that easily and reliably find early-stages of pancreatic cancer in people, sometimes show no symptoms.Often “times it is” not found until later stages when the cancer can no longer be surgically removed and has spread from the pancreas to other parts of the body. ("Pancreatic Cancer: Statistics", 2017)

Cirrhosis is the eighth leading cause of death in the United States and the thirteenth leading cause of death worldwide.1 Cirrhosis is the irreversible fibrosis of the liver characterized by hepatic architectural distortion secondary to fibrous tissue and the formation of regenerative nodules.2 These anatomical changes cause hepatic vascular resistance and an increase in blood flow leading to portal hypertension. Porto-systemic collaterals develop in order to overcome the increased portal pressure gradient.3 Nitric oxide, an endogenous vasodilator is also released in effort to overcome portal pressure with the expense of causing systemic vasodilation and a decrease in blood pressure. As a result, a marked activation of neurohumoral vasoactive factors occurs in an effort to maintain an effective arterial blood pressure. Hypervolemia, increased cardiac index, decreased systemic vascular resistance, and systemic hypotension are manifestations of portal hypertension.3 Chronic hepatitis B virus (HBV), hepatitis C virus (HCV), alcoholism, nonalcoholic steatohepatitis (NASH), and non-alcoholic fatty liver disease (NAFLD) are all major causes of cirrhosis.

Venous thromboembolism refers to the formation of a blood clot in a blood vessel. While clots can form in an artery or a vein, this article focuses only on clots that occur in a vein ("," 2015). Critically ill patients are at an increased risk of a venous thromboembolism (VTE) due to VTE can manifest as a deep venous thrombosis (DVT) or a pulmonary embolism (PE). Risk factors include venous stasis, vascular injury, and hypercoagulable disorders. A majority of ICU patients carry at least one risk factor for VTE; additional risk factors are considered to have a cumulative effect…it is impossible to predict which patients will experience a

A DVT is a thrombus or blood clot that most commonly occurs in deep veins in the leg or pelvis. DVTs usually start distally in the veins of

Venous Thromboembolism (VTE) is a disease that embodies both pulmonary embolism (PE) and deep vein thrombosis (DVT). On the side of research, VTE is the most common preventable cause of hospital-associated mortality and is both the second most common medical complication and cause of excess length of hospital stay (LOS). Furthermore, with appropriate evidence-based prophylactic measures, the occurrence of hospital-associated VTE (HA-VTE) can be reduced by as much as seventy percent. Subsequently, there are approximately between 200,000 and 300,000 VTE-related deaths annually, which is greater than the yearly rate of mortality for breast cancer,

There are many people that suffer from venous thromboembolism. Venous thromboembolism includes both deep vein thrombosis and pulmonary embolism. This is the third most common cause of vascular death after a myocardial infarction, also known as a heart attack, and stroke. This article examines the possibility of either full or low intensity anticoagulation therapy versus aspirin. This was a randomized study that consisted of 3,396 individuals who have venous thromboembolism. These individuals either received rivaroxaban, which is an anticoagulant, or 100 mg of aspirin once a day. The individuals in this study completed 6-12 months of anticoagulation therapy and were eligible for inclusion in the study if they were 18 years of age or older. The

Venous thromboembolism (VTE) is an epidemic that rain rapid in Australia and was a very big concern. The study of this sickness was a major Problem as it had affected the demographic area of Perth, Australia. The epidemic is a very big problem as VTE is connected with the trauma, surgery, and cancer and this sickness is caused while

Enoxaparin is a low molecular weight heparin used to prevent thrombosis, particularly post surgery. Enoxaparin binds to antithrombin III which is responsible for inhibiting coagulation by acting on factor Xa. Enoxaparin accelerates the activity of antithrombin III therefore preventing clot formation (McKenna & Lim, 2014 p766). When a blood vessel is damaged, platelets in circulating blood stick to the site of injury and release chemicals that attract more platelets causing aggregation. There are both intrinsic and extrinsic pathways causing thrombi to form to maintain a closed cardiovascular system (Hollar, 2017). Immobility increases risk of thrombus formation as the blood becomes stagnant with gravity and decreased

Anticoagulants are a type of drug that reduces the body’s ability to form blood clots in the blood by inhibiting the production of vitamin K in the liver. The goals of the anticoagulant therapy are to prevent stroke in patients with atrial fibrillation and artificial heart valves. In patients with PE/DVT, the primary goal of the anticoagulant is to prevent an existing clot from getting larger. Anticoagulant drugs can be used after surgery to prevent new blood clots. Anticoagulant drugs increase the risk of bleeding. Because of this risk, it is essentially important to educate the patient to take the medication exactly as directed and never take larger or more frequent doses. The challenges of anticoagulant therapy are to keep it in the therapeutic

Thrombolytic therapy is the use of drugs to break up or dissolve blood clots, which are the main cause of both heart attacks and stroke.

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.

Thrombin is a naturally occurring protein that is present in the blood of humans and animals. The main function of thrombin is as an intermediate step during hemostasis, which slows bleeding by forming blood clots. Thrombin acts as an enzyme during an injury, converting fibrinogen to fibrin, which then causes blood clots to form. Due to its properties, thrombin’s application to the medical field includes topical surgery in the case of minor injuries as well as various other medical procedures such as neurosurgical operations. Apart from applications in the medical field, thrombin also plays significant roles by directly interacting with endothelial cells throughout the body.

Cancer is a well known disease with high mortality and morbidity. The morbidity and mortality may be further increased by certain comorbidities that may abate the effectiveness of the treatment regime and increase the burden imposed. One such well recognised comorbidity is thrombosis and the association between the two was first described in 1823 by Jean-Baptiste Bouillard [1]. Later studies by French physician, Armand Trousseau, reported the association between gastric cancer and thrombosis in 1865 [2], however, it was only in 1935 that thrombosis was reported as a first sign of an occult cancer [3].