Pathology of Deep Venous Thrombosis

Deep Vein Thrombosis (DVT) is a serious medical condition that affects certain hospitalized patients. The healthcare team, especially the registered nurse, must understand what this condition entails, who it affects, and how to prevent and treat this condition. The proper knowledge and training will allow the registered nurse to be able to keep the patients safe and help prevent complication from deep vein thrombosis.

Ventricular septal defect cause the blood flow move from high pressure, left ventricle, into the right ventricle, which has lower pressure. Oxygenated blood instead of going to the systemic circulation enters into the left ventricle and goes into the pulmonary artery and to the lungs. As the result return of the blood from the lungs to the left atrium and eventually into the left ventricle, will increase and cause dilation and hypertrophy of the chambers, increases end-diastolic pressure, and raise the pulmonary venous pressure. By increasing the pulmonary blood flow, the pulmonary capillary pressure also rises and that can increase the interstitial fluid in the lungs, and cause pulmonary edema. Finally, as blood goes through the gap, from the LV to the RV, away from the aorta, case the cardiac output to drop,

The clinical picture of acute pulmonary embolism (PE) is not similar from various aspect of its pathophysiological course presenting from minimal symptoms to variety of severity of disease like severe hypoxia, hypotension, right heart failure and death1. Massive pulmonary embolism is defined as obstruction of blood flow to a lobe or multiple segments of the lung, or for unstable hemodynamics, i.e. failure to maintain blood pressure without supportive measures.” This case highlights about aggressiveness of treatment and role of thrombolytic therapy for a severely hemodynamic unstable patient2.

Patients who experience prolonged bed rest, older than 40, and are obese are even more likely to develop pulmonary embolism as a secondary diagnosis. Predisposing disorders that can increase the risk of pulmonary embolism are cardiac arrhythmia, lung disorders, cardiac disorders, diabetes mellitus, and more (Wolters Kluwer, 2017).

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

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

Konstantinides, S., & Goldhaber, S. (2012). Pulmonary embolism: Risk assessment and management. European Heart Journal, 33(24), 3014-3022.

This abnormality causes the aorta to arise from the right ventricle and the pulmonary artery to arise from the left ventricle, which is opposite if normal anatomy.2 Patients may also present with narrowing of the pulmonary artery, hypertrophy of the right ventricle and atrophy of the left ventricle. TGA causes decreased oxygen supply to the body because deoxygenated blood from the right ventricles never reaches the lungs to be re-oxygenated. Oxygenated blood from the left ventricle does go to the lungs but is in a closed system so never pumps through the body, thus causing cyanosis, shortness of breath and decreased feeding in patients.4,5 In some patients a bidirectional shunt is present allowing mixing of oxygenated and deoxygenated blood, however patients with no shunt will need surgical intervention in order to alleviate

The prevalence for PE was estimated to be around 24.5% and DVT was 15% at the HEGP University Hospital, considering all patients with suspected embolism. Besides, these CT imaging procedures also help in detecting clinically significant non-vascular findings such as lesions that are implied as incidental imaging findings. It was observed that F- measure for the detection of pulmonary embolism is 0.98, deep vein thrombosis is 1.00 and clinically relevant incidental findings is 0.80. This represents that both the imaging techniques are equally potential in contributing to the diagnosis of thromboembolic

Superior vena cava (SVC) syndrome results from any condition that leads to obstruction of blood flow through the SVC. Obstruction can be caused by invasion or external compression of the SVC by adjacent pathologic processes involving the right lung, lymph nodes, and other mediastinal structures, or by thrombosis of blood within the SVC. In some cases, both external compression and thrombosis coexist [ 1] .

A Deep Venous Thrombosis (DVT) will propagate when there is either stasis of blood flow, endothelial injury, or if the patient is in a hypercoagulable state. Under physiological conditions, a dislodged DVT can predictably settle in the pulmonary arteries causing a pulmonary embolism. However, a DVT in the presence of a intracardiac shunt or PAVM can paradoxically cause an embolism in branches of the aorta. The pathophysiological mechanism varies depending on the etiology of the paradoxical embolism. For instance, in a paradoxical embolism due to a PFO, a DVT gets dislodged and enters the right atrium where a transient increase in right atrial pressure during a Valsalva maneuver can force the embolism through the PFO and into the left atrium

Representatives from Thrombolysis in Myocardial Infarction (TIMI), Duke Clinical Research Institute (DCRI), and Merck & Co., Inc.

Compression stockings and brief walks to promote blood circulation can aid in resolving and also preventing DVTs. Findings from clinical trials have shown the effectiveness and safety of pharmacological prevention with low, fixed doses of anticoagulant drugs (Goldhaber). “Although approximately half of venous thrombotic events treated with traditional anticoagulant blood thinners resolve during a 3 to 6 month conventional duration, the risk of Post Thrombotic syndrome (PTS) persists, possibly due to acute valvular damage from complete venous obstruction (Greene). Anticoagulants have been recommended for at least 3 months, though duration of this therapy should be based on the risk of recurrence as well as whether the blood clot has

Echocardiography can underestimate the degree of PVS, because blood flow is redistributed toward the less-obstructed portions of the lung, resulting in decreased flow through the stenotic vein.81 Alternatively, the pulmonary veins may have been normal initially, and the stenosis developed over time.3,5 While most studies continue to use echocardiography as the primary modality in the diagnosis of PVS8, potential advantages of cardiac CT or MRI include better delineation of pulmonary venous anatomy and blood flow distribution.79 To answer questions on the timing and nature of disease progression, more uniform methods of diagnosis surveillance, with pre-specified cut-off values for defining PVS, are needed.1,79,82