الفهرس 
Risk and Pathophysiology of Postoperative Venous ThromboembolismOnly 14 pages are availabe for public view
 |  | from | 120 |  |  |
| | | from | 120 | | |
Abstract
Deep venous thrombosis (DVT) and pulmonary embolism (PE)are components of a single disease termed venous thromboembolism (VTE) .
Embolisation of DVT to the pulmonary arteries leads to PE, which is the most severe and life-threatening manifestation., VTE occurs in the population at a rate of about 1 in 1000 per year and is more common both with advancing age and in males. Most PE results from DVT of the lower limbs, pelvic veins or inferior vena cava (IVC), although DVT of the upper limbs, right atrium or ventricle does also occur. Up to 40% of patients with DVT develop PE.
Despite a better understanding of the pathophysiology of VTE, improvements in diagnostic approaches and techniques, extensive clinical research of treatment options, and widespread recognition of the importance of DVT prevention, VTE continues to be a common and life-threatening problem. It has been estimated that acute PE accounts for 5-10% of deaths among hospitalized patients and that up to three million persons die of PE annually in the United States 70% of which are not recognized antemortem.
Predisposing risk factors for VTE involve one or more components of Virchow’s triad : (1) venous stasis; (2) vein wall injury; and (3) hypercoagulability of blood. The main factors are immobility (from any cause), surgery, trauma, malignancy, pregnancy and thrombophilia .
The effects of PE range from being incidental and clinically irrelevant to causing severe obstruction to the pulmonary circulation.
Risk factors for VTE can be acquired, inherited, or mixed. An underlying cause for thrombosis can currently be identified in up to 80% of cases.
A patient’s symptoms and physical examination cannot be used to confirm or exclude the diagnosis of DVT. The presence of erythema, warmth, pain, swellin or tenderness may suggest the presence of DVT but lack of these findings does not exclude the diagnosis.
The most common symptoms/ signs of PE are dyspnea, tachypnea, and tachycardia are seen with a myriad of other disorders A more frequent presentation of PE is acute onset of shortness of breath or hypoxemia, with or without chest pain .
Contrast venography has long been the diagnostic standard in thromboprophylaxis trials because of its high sensitivity for detecting DVT and the availability. Venous Doppler ultrasonography (DUS) is now the most universally accepted test for the diagnosis of lower extremity DVT, because it is highly accurate for symptomatic DVT, widely available, and noninvasive.
Unless there is a serious contraindication, nearly all patients should receive anticoagulation with either unfractionated or low-molecular-weight heparin (LMWH) to prevent VTE recurrence.
The most powerful statement that can be made for prophylaxis is that, of the patients who die of pulmonary emboli, most patients survive 30 min after the event, which is not long for most forms of treatment to be effective. Without prophylaxis, the frequency of fatal PE is markedly high.
The belief that routine thromboprophylaxis is mainly justified by the reduction in the rate of fatal PE does not address the non-fatal complications of deep vein thrombosis. There is significant risk of long-term morbidity from post-thrombotic venous insufficiency and chronic venous ulcers. The concern over bleeding is often given as the main reason for withholding therapy. The clinical benefit and cost-effectiveness of thromboprophylaxis can be maximized by accurate assessment of patients’ risk factors for the development of VTE.