Abdiraimov iskender sir - Deep vein thrombosis and and pulmonary embolism

Deep vein thrombosis and and pulmonary embolism ABSTRACT : Deep vein thrombosis (DVT) is an important preventable cause of morbidity and mortality throughout the world. Venous thromboembolism (VTE), which includes DVT and pulmonary embolism (PE), affects an estimated 1 per 1,000 people and causes 60,000–100,000 deaths annually. The physiology of normal blood relies on a delicate balance between pro- and anti-coagulant factors. Virchow's Triad, however, condenses the myriad of risk factors for DVT into three basic elements favoring thrombus development: venous stasis, vascular injury, and hypercoagulability. These clinical, biochemical, and radiological studies help to increase the sensitivity and specificity for DVT diagnosis. Anticoagulant therapy forms the mainstay in the treatment of DVT. With a few exceptions, the standard treatment of DVT has been VKAs such as warfarin with heparin or fractionated heparin bridging. In the more recent past, a number of large clinical trials have established the usefulness of DOACs as an alternative to warfarin in some circumstances. In this article, we discuss the pathogenesis, diagnosis, and medical management of DVT, with particular emphasis on anticoagulation therapy and the role of DOACs in the current treatment landscape. INTRODUCTION : Deep vein thrombosis (DVT), a type of venous thromboembolism (VTE), is a major preventable cause of morbidity and mortality worldwide. VTE is estimated to have an incidence of 1 per 1,000 individuals annually , with DVT accounting for approximately two-thirds of events . Pulmonary embolism (PE), the dreaded complication of DVT, occurs in up to one-third of patients and is the most common cause of death . The majority of morbidity due to DVT occurs due to the development of post-thrombotic syndrome, which in as many as 50% of patients within 2 years of DVT comprises a constellation of symptoms that encompass leg pain, swelling, and in severe instances, venous ulcers . Management of DVT depends on anticoagulation as the mainstay of treatment, with the objective being prevention of extension to PE and recurrence of thrombosis. Mortality within 30 days of DVT is over 3% in patients with DVT who are not anticoagulated, and this mortality risk is 10-fold greater in those patients who proceed to develop PE . The advent of direct oral anticoagulants (DOACs) has necessitated the need to compare these newer agents with the more established vitamin K-antagonists (VKAs) for the treatment of DVT. Several recently completed clinical trials have resolved this question and demonstrated a similar safety and efficacy profile of both classes of agents. With more therapeutic options, clinicians are now better able to include disease- and patient-specific factors in the medical management of DVT KEYWORDS : symptoms , treatment , summary , conculsion CAUSES Anything that prevents the blood from flowing or properly clotting can cause a blood clot. The main causes of deep vein thrombosis (DVT) are damage to a vein from surgery or inflammation and damage due to infection or injury. SYMPTOMS : * Deep Vein Thrombosis (DVT) A DVT usually occurs in the deep veins of the legs (less often in the arms). Common Symptoms *Swelling of the affected leg (rarely both legs)Pain or tenderness in the leg — often in the calf or thigh Warmth over the area of the clot * Red or discolored skin Heaviness or tightness in the leg * Less common / late signs *Veins near the skin may become more visible or distended *Low-grade fever sometimes present * Pulmonary Embolism (PE) A PE occurs when part of a DVT breaks off and travels to the lungs, blocking blood flow. Common Symptoms *Sudden shortness of breath (even at rest) Chest pain — sharp or stabbing, worsens with deep breathing or coughing *Cough (may produce bloody or blood-streaked sputum) *Rapid heart rate (tachycardia) *Rapid breathing (tachypnea) Other possible signs *Feeling lightheaded, dizzy, or faint (syncope) *Low oxygen levels (hypoxia) *Anxiety or sense of impending doom *Bluish skin (cyanosis) in severe cases TREATMENT * Main Goal of Treatment *Prevent the clot from growing. *Stop the clot from traveling to the lungs (prevent PE). *Prevent new clots from forming. *Reduce long-term complications (like post-thrombotic syndrome or chronic thromboembolic pulmonary hypertension). 2. Anticoagulation (Blood Thinners) — Mainstay of Treatment First-line: Direct Oral Anticoagulants (DOACs) Examples: *Apixaban (Eliquis) *Rivaroxaban (Xarelto) *Edoxaban *Dabigatran (Pradaxa) Alternative: Heparin-based Therapy Unfractionated Heparin (UFH) – IV infusion, used in hospital or in unstable PE (easy to reverse). Low Molecular Weight Heparin (LMWH) – e.g., Enoxaparin (Clexane), Dalteparin, given by injection. *Transition to Warfarin (if used) *Warfarin (Coumadin) is used less often now. *Requires INR monitoring (target 2.0–3.0). *Usually bridged with heparin until INR is therapeutic. Duration of Treatment * Provoked DVT/PE (temporary risk factor, e.g., surgery): 3 months * Unprovoked DVT/PE: 6–12 months or longer Recurrent or ongoing risk (e.g., cancer, inherited thrombophilia): May need lifelong anticoagulation 3. Thrombolytic (Clot-Dissolving) Therapy Used only in severe or life-threatening cases, such as: Massive PE causing shock or severe hypoxia Extensive DVT (e.g., phlegmasia cerulea dolens) Drugs: Alteplase (tPA) or other tissue plasminogen activators Dissolves clots rapidly but carries a high risk of bleeding. 4. Surgical / Interventional Options Catheter-directed thrombolysis: Delivers clot-busting drugs directly into the clot. Thrombectomy: Mechanical removal of the clot (for large, limb-threatening DVT or massive PE). IVC (Inferior Vena Cava) Filter: Used only if anticoagulation is contraindicated (e.g., recent brain bleed, major trauma). SUMMARY DVT is an everyday and infuriating problem for doctors. Normal hemostasis of blood allows for coagulation in the appropriate setting, but several disease processes can disrupt pro- and anti-coagulant homeostasis to create pathologic formation of thrombus. DVT is more accurately diagnosed with the Wells score, d-dimer assay, and a growing array of imaging studies such as US, CT, and MR venography. Treatment of DVT has traditionally included VKAs such as warfarin with heparin or bridging with fractionated heparin . With the advent of DOACs came hope for additional therapies for DVT but safety and efficacy profile of newer agents vs conventional therapy has been of paramount concern. After more than a decade of research, multiple large-scale clinical trials have demonstrated comparable efficacy between the two drug classes . Although the safety profile for DOACs has been quite favorable, dabigatran and rivaroxaban have been associated with an increased risk of GI bleeding in select patients . Conversely, apixaban and edoxaban were associated with a lower risk of non-major bleeding in the AMPLIFY and HOKUSAI-VTE trials, respectively . In patients who are on dabigatran for stroke and DVT prophylaxis, and acute coronary syndrome (ACS), a greater risk of myocardial infarction has been found . DOACs are as effective as warfarin in the management of DVT overall. DOACs are employed with caution in some patient groups like older patients, with atrial fibrillation or other cardiac risk factors, or at increased risk of GI bleeding. CONCLUSION Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE) are two conditions of venous thromboembolism (VTE), a disease that, unless diagnosed and treated in due course, can prove to be life-threatening.Early diagnosis of signs of DVT such as swelling, tenderness, and redness in the leg or sudden shortness of breath and chest pain (PE) prevents complications.Anticoagulation therapy remains the pillar of therapy, preventing extension and recurrence of the clot effectively. Thrombolysis or surgery could be required in extensive or massive thrombosis.With early diagnosis, appropriate treatment, and preventive factors (e.g., mobilization, hydration, and prophylactic anticoagulant administration in high-risk patients), the prognosis is also good and the risk of recurrence or death can be significantly reduced. References 1.Beckman MG, Hooper WC, Critchley SE, et al. Venous thromboembolism: a public health concern. Am J Prev Med 2010;38:S495-501. 10.1016/j.amepre.2009.12.017 2.White RH. The epidemiology of venous thromboembolism. Circulation 2003;107:I4-8. 10.1161/01.CIR.0000078468.11849.66 3.Silverstein MD, Heit JA, Mohr DN, et al. Trends in the incidence of deep vein thrombosis and pulmonary embolism: a 25-year population-based study. Arch Intern Med 1998;158:585-93. 10.1001/archinte.158.6.585 4.Kearon C. Natural history of venous thromboembolism. Circulation 2003;107:I22-30. 10.1161/01.CIR.0000078464.82671.78 Kearon C, et al. 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