Diseases of Veins

By | 2013-07-19

Diseases of the venous system frequently cause minor clinical problems, despite the fact that veins are commonly affected by or involved in trauma, TE, edema, local inflammation, and septic processes. Many conditions, however, often go unrecognized. Venous disorders include traumatic injuries, superficial and deep phlebitis and thrombosis (thrombophlebitis), catheter embolization, aneurysms, venous compression syndromes, varices, and ulcers.

Pulmonary thromboembolism (PTE) is a common and often life-threatening complication associated with a variety of systemic and metabolic diseases. A thrombus formed in the right heart or the peripheral or central venous system can embolize to the pulmonary arterial vasculature. Contributing factors include prolonged immobilization, trauma, surgery, and a range of disorders including IMHA, hyperadrenocorticism, nephrotic syndrome, DIC, sepsis, cardiac disease, amyloidosis, neoplasia, proteins C and S deficiency, and antithrombin III deficiency. postadulticidal thromboembolization is covered in detail in site.

Varicosis and ulceration are rare in dogs and cats. When detected, they often accompany A-V fistulas. Cutaneous phlebectasia is a benign lesion sometimes erroneously called telangiectasis. It is reported almost exclusively in dogs with spontaneous or iatrogenic Cushing’s syndrome. Phlebectasia is an abnormal dilatation, extension, or reduplication of veins or capillaries or a combination of these changes.

Venous perforation or blunt trauma to veins is usually well tolerated because rapid clotting results in venous occlusion. If when venous occlusion or venous severance is severe, however, resultant edema and cyanosis are usually temporary because of collateral circulation. If all veins.draining an area are compromised, marked edema and necrosis can ensue. Blunt trauma has been associated with caudal vena caval obstruction or kinking of the intrathoracic caudal vena cava and ascites.

Venous malformations have been previously referred to as cavernous hemangiomas. They can be localized or extensive and appear as cystic dilation of blood vessels. They generally permit only low blood flow, and small lesions are generally asymptomatic. Expansion of the lesion may occur, however, especially after trauma. Thrombosis may occur due to sluggish blood flow, resulting in local swelling and tenderness. Larger lesions in dependent areas may enlarge, causing significant vascular dilation. Tliis may result in changes in skin color, ulceration, and hemorrhage. The affected area appears as a warm, soft, compressible mass. No thrills or bruits are present due to the low flow. Pain may result from pressure exerted on deep tissues and nerves.

Diagnosis is made using history, physical examination, and ultrasound. Venography may be needed to define the lesion. Symptomatic therapy using light, compressive wraps is sometimes helpful for acute management. Surgical excision of affected vessels is occasionally required, but complete resection is difficult and local recurrence is common.

Thrombosis commonly follows blunt trauma and perforating injuries, particularly with venipuncture or prolonged venous catheterization. Phlebitis is a major cause of intimal damage leading to thrombosis. The thrombosis is usually of little local consequence. However, emboli may be carried to the lung and cause PTE. In most animals, blood clots carried to the lung are rapidly lysed and cause no problems. However, when inflammatory diseases, dehydration, or circulatory failure occurs, clot formation may continue in the pulmonary vessels and lead to vascular occlusion, severe dyspnea, pain, and death. In infectious thrombophlebitis, bacterial emboli may be carried to the lungs and cause thromboembolic pneumonia. Spontaneous venous thrombosis is rare, although portal vein thrombosis has been reported. Clinical signs include ascites, peripheral pitting edema, and portosystemic shunting.

Embolization of severed intravascular catheter fragments is an occasional complication of intravenous catheter placement. In humans, reported complications of catheter embolization include perforation of cardiac walls, endocarditis, pulmonary embolism, and severe arrhythmias. Therefore it is generally considered prudent to remove catheter fragments. Nonsurgical, transvenous removal of catheter fragments using loop-snare catheters, forceps, and basket catheters have been described. Whenever possible, however, steps should be taken to avoid situations predisposing to catheter fragmentation, including inadequate restraint during catheter placement, withdrawal of catheters through their placement needles during repositioning, failure to properly secure catheter to the patient, and inadvertent severing of catheters during bandage changes.

Phlebitis can occur from a local inflammatory process extending to the veins or can originate from a venous intimal lesion. Common causes of venous intimal lesions are perive-nous injection of irritating drugs, infusion of large amounts of fluid, and long-term placement of intravenous catheters. Infusion-related phlebitis occurs in three forms: (1) chemical (injury to vein by irritating drugs), (2) physical (trauma to the intima by catheters, needles, nypertonicity, or particulate matter in infused fluids), and (3) microbial (infected fluids, skin, or catheter tip). Sterile or septic thrombophlebitis may result, usually remains localized, and is characterized by pain, swelling, and exudation. Patients with serious illnesses or compromised immune systems, however, may develop sepsis, thromboembolic pneumonia, or endocarditis.

In cases of venous occlusion, clinical signs depend on the anatomic location, extent, and duration of the obstruction. Acute obstruction of centrally located and deep veins causes edema, cyanosis, discomfort, and venous dilatation distal to the obstruction site. Obstruction of the cranial vena cava causes edema in the neck, head, front limbs, and dependent portions of the chest wall. Pleura! effusion commonly results from central venous obstruction. Clinical disorders of the intrathoracic caudal vena cava have been reported. Obstructions of the renal or pelvic area cause edema of the hindlimbs and the scrotum. Clinical signs depend upon collateral vessel reserve and capacity of regional lymphatics. In addition to thrombosis, common causes of venous obstruction include invasive malignant processes and venous compression by abscesses, hematomas, tumors, and Iymphadenopathy. A number of tumors have a tendency for venous invasion, including chemodectomas, adrenal tumors, and hemangiosarcomas. Angiography may indicate the occlusive or compressive lesion or highlight increased collateral circulation (or it may do both). Diagnostic ultrasonography can often detect masses or flow disturbances.

The prognosis and therapy of venous obstruction depend on the primary disease.