Venous Thromboembolism

Venous Thromboembolism

Introduction

Deep vein thrombosis is a common disease that can develop subclinical or debut as an acute edema, congestion and limb pain, sometimes disabling. In addition to local problems, the main risk is pulmonary embolism, which can be fatal. Deep vein thrombosis leaves local consequences in the long term can cause secondary varicose veins, trophic skin changes and venous ulcers. These disorders are of absenteeism and even disability. Knowledge of the predisposing factors allows us to avoid the development of venous thrombosis and its complications. Prevention is based on simple, highly effective measures, so we assign as much or more important than treatment of established disease.

Discussion

A mid 19th century Virchow stated the three key factors in the pathogenesis of intravascular thrombosis: vascular wall damage, stasis of blood flow and changes in blood coagulability. Today, close to 21 century and that definition continues. Epidemiological studies, age over 50 years, obesity, hypertension and smoking are factors associated with increased risk of vein thrombosis. Blunt trauma to the vascular endothelium may occur during some diagnostic and therapeutic procedures performed by femoral venous line e.g. venous catheter for dialysis, cardiac studies, etc. The prolonged venous catheterization for chemotherapy, parenteral hyper alimentation or monitoring, can give rise to phlebothrombosis, despite the use of non-thrombogenic catheter material.

Indirect trauma to the vein wall may occur in bruises and fractures. Recent studies have shown phlebothrombosis between 50 and 70% of patients with major trauma trunk or lower extremities, venous endothelial injury being a predisposing initial element.

Thrombosis can also be induced by activation of endothelial cells by cytokines from traumatic or inflammatory processes remotely.

Surgical procedures, especially orthopedic for arthroplasties e.g. hip or knee, or operations of the pelvic cavity e.g. gynecological and urological are associated with an increased risk of vein thrombosis, which is attributed to damage to neighboring venous structures. Endothelial damage, sequel to a previous phlebothrombosis is also a predisposing factor for a new phlebothrombosis.

Decreased venous flow rate is a factor favoring flebotrombosis. The slowdown is normal at rest and muscular immobility, so the single prolonged bed rest may be a predisposing cause. The slow venous return may also have its origin in a central disorder with decreased cardiac output, as occurs in heart failure.

The forced stillness, with no muscle function, extended trips pump itself without the possibility of wandering, immobilization of a limb sprain or fracture, immobility of both limbs neurological brain or spinal injury, immobility by admin general or regional anesthesia, are all conditions that share the same common predisposing factor: the lower flow rate of venous return.

Phlebothrombosis risk by slowing blood flow occurs if extrinsic venous compression, frequent situation in pregnancy and less frequently tumors or retroperitoneal or pelvic masses (Findlay et al., 2010).

Venous dilatation is deep surface area or post-thrombotic squeal, venous insufficiency and venous aneurysms are also a factor associated with venous stasis thrombosis. Blood remains in a liquid state by the balance between procoagulant factors and anticoagulant factors. This balance can be ...