Chapter 21 Venous and Lymphatic Disease

Principles of Surgery Companion Handbook


Anatomy of the Venous System
Deep Venous Thrombosis
 Chronic Venous Insufficiency
 Inferior Vena Caval Interruption
 Other Types of Venous Thrombosis
Pulmonary Embolism
Varicose Veins


The veins of the extremities are divided into three systems. There is a deep system, below the level of the fascia of the muscles. The valves in the deep system serve to direct blood flow toward the heart. There is a superficial system, residing in the subcutaneous tissue of the extremities. The valves in the superficial system also are oriented so that the direction of blood flow is toward the heart. Finally, there is a system of communicating veins connecting the superficial system with the deep system. The communicating veins have valves oriented so that the flow of blood is from the superficial to the deep system. The communicating veins are most prominent along the medial aspect of the calf, where they are known as perforating veins.

The flow of blood in veins is phasic with respiration. During inspiration, abdominal pressure increases, and venous flow in the lower extremities decreases transiently. During expiration, abdominal pressure decreases, and lower extremity venous flow increases. The “calf muscle pump” facilitates the flow of blood back to the heart. Within the muscle of the calf, venous sinuses exist, most prominently in the soleus and gastrocnemius muscles. With each contraction of the calf muscles, blood is forced into the longitudinally oriented deep veins, and the valves preferentially direct the flow toward the heart. In the absence of competent venous valves, however, muscle contraction forces blood in all directions. Incompetent communicating veins are especially problematic because calf muscle contraction ejects blood in a retrograde direction through the communicators. These spurts of blood with each contraction of the muscle produce localized venous hypertension, edema, and rupture of small venules in the subcutaneous tissue overlying the communicators—the genesis of the skin (hemosiderin deposits and ulceration) and subcutaneous changes (brawny edema and fibrosis) associated with chronic venous insufficiency.


Virchow postulated three mechanisms for the development of venous thrombosis: endothelial damage, hypercoagulability, and stasis. These factors account for the high incidence of deep venous thrombosis (DVT) after an operation. Thrombi that form in areas of rapidly flowing blood (arteries) are generally gray in color and primarily composed of platelets. By contrast, thrombi occurring in relatively slowly flowing systems (veins) are red and primarily composed of fibrin and red blood cells.

Etiology of Deep Venous Thrombosis

  1. Endothelial cell damage
    1. Immune vasculitis
      1. Systemic lupus erythematosus
      2. Buerger's disease
      3. Giant cell arteritis
      4. Takayasu disease
      5. Vasculitis with anticardiolipin factor
  2. Hypercoagulability
    1. Activated protein C resistance
    2. Antiphospholipid syndrome
    3. Antithrombin III deficiency
    4. Protein C and S deficiencies
    5. Dysfibrinogenemia
  3. Stasis
    1. Congestive heart failure
    2. Hyperviscosity
    3. Prolonged immobility (bed rest, airplane and automobile trips)
    4. Neurologic disorders with loss of muscle pump

Diagnosis of Deep Venous Thrombosis The clinical diagnosis of DVT is notoriously inaccurate, and objective tests have become the cornerstone of diagnosis. Contrast phlebography is the “gold standard” test. Duplex ultrasound is very accurate, especially when the patient is symptomatic or the thrombus is present in the femoral segment. Duplex is less sensitive for isolated thrombi of the calf veins or of the iliac veins. Isolated iliac vein thrombosis is rare.

Prophylaxis of Deep Venous Thrombosis Patients at high risk for venous thrombotic events can be treated with a variety of means to diminish the chance of deep venous thrombosis. These patient groups include those undergoing major operative procedures, particularly orthopedic procedures. Other high-risk groups include patients with malignancy, major trauma, paralysis, and a history of previous DVT. The following represent prophylactic methods used in these high-risk groups:

  1. Elastic compression stockings to reduce stasis
  2. Intermittent pneumatic compression to reduce stasis and enhance intrinsic fibrinolysis
  3. Low-dose subcutaneous heparin administration
  4. Low-molecular-weight heparin administration
  5. Warfarin anticoagulation in patients undergoing major joint replacement

Treatment of Deep Venous Thrombosis The treatment of deep venous thrombosis depends on the location of the thrombus. Isolated calf vein thrombi may be treated without anticoagulation, especially if they develop as a result of an identifiable event such as trauma or surgery. De novo calf vein thrombi may represent a hypercoagulable state, whether identified or not, and anticoagulation is prudent. Proximal deep venous thrombi should be treated with anticoagulation to prevent propagation of thrombus and pulmonary embolism. Therapy is begun with intravenous heparin, with the goal of achieving an activated partial thromboplastin time (APTT) of more than two times control. Oral anticoagulation with warfarin can be instituted concurrently, aiming for an international normalized ratio (INR) of approximately 2.0. Heparin may be discontinued after the INR stabilizes at a therapeutic level.

As an alternative to intravenous heparin, subcutaneous low-molecular-weight heparin (LMWH) therapy has been used successfully on an outpatient, ambulatory basis. APTTs are not assessed with LMWH; their use is meaningless because LMWH does not reproducibly alter the APTT. Randomized studies have not detected an increased frequency of pulmonary embolism with outpatient LMWH therapy for DVT.

Chronic Venous Insufficiency

Chronic venous insufficiency, also known as the postthrombotic or postphlebitic syndrome, develops in the majority of patients who have sustained a significant DVT. The underlying pathophysiology consists of recanalization of the deep system with subsequent incompetence of the valves. The high venous pressure then promotes fluid and protein loss into the subcutaneous tissues, resulting in subcutaneous fibrosis probably secondary to inadequate tissue oxygenation and metabolism. This “liposclerosis” produces the brawny edema characteristic of the postphlebitic syndrome. Chronic microscopic hemorrhage into these tissues produces deposition of hemosiderin and the characteristic brown pigmentation. Ulceration occurs frequently and generally is located above the medial malleolus. The chronic edema predisposes the patient to recurrent bouts of cellulitis. The therapy of chronic venous insufficiency is supportive initially. Compression stockings usually are used, as is bed rest with leg elevation and paste boots. Operative therapy is reserved for patients with persistent ulceration despite adequate conservative measures. The perforating veins may be ligated, usually via a subfascial approach; however, wound infection and recurrent ulceration frequently accompany this procedure. An endoscopic method of perforating vein ligation has been developed, and the initial results are promising. Venous reconstruction is indicated in a minority of patients with nonhealing venous ulceration. Ascending and descending phlebography and ambulatory venous pressure measurements are mandatory in determining whether patients are candidates for venous reconstructive procedures. Venous valve repair (congenital incompetence) and venous valve transposition (acquired incompetence) have been used in patients with pure valvular incompetence without outflow obstruction, whereas a number of venous bypass techniques have been used in others with documented, persistent venous hypertension.

Inferior Vena Caval Interruption

Vena caval interruption has been used in an effort to prevent pulmonary emboli. The procedure is percutaneous, with the introduction of a variety of filters into the inferior vena cava. The indications for vena caval interruption include pulmonary embolus with a contraindication for anticoagulation, recurrent pulmonary embolism on adequate anticoagulation, and as prophylaxis against recurrent embolism after pulmonary embolectomy. A relative indication for caval interruption occurs in patients with large iliofemoral DVT with a contraindication to anticoagulation.

Other Types of Venous Thrombosis

Superficial Thrombophlebitis This process is characterized by aseptic thrombosis of the superficial veins. In the lower extremities, it usually is associated with varicose veins, occasionally after trivial trauma, and it is dangerous only when it propagates to the common femoral vein. Therapy is usually supportive, including bed rest, warm packs, and anti-inflammatory agents. Superficial thrombophlebitis in the upper limbs usually is secondary to intravenous infusions. Excision of the vein is indicated when the process is purulent.

Subclavian Vein Thrombosis Thrombosis of the subclavian vein occurs in two settings. The first is in the presence of an indwelling catheter. Removal of the catheter is indicated. It also may occur as an “effort thrombosis,” usually in the setting of thoracic outlet syndrome. Thrombolytic therapy has been helpful when an effort thrombosis occurs, and subsequent thoracic outlet decompression (clavicle or first rib resection) with or without venous reconstruction (patch angioplasty or venous bypass) frequently is necessary.


Diagnosis of Pulmonary Embolism A patient with a pulmonary embolism classically presents with chest pain, cough, dyspnea, and tachypnea. Hemoptysis occurs late and is associated with pulmonary infarction. The electrocardiogram (ECG) and chest radiographs are used primarily to exclude other diagnoses. Arterial blood gases usually reveal room air PO2 below 60 mmHg and decreased PCO2. If a Swan-Ganz catheter is placed, the pulmonary arterial pressures frequently are elevated, and the wedge pressure is normal or diminished (Table 21-1).


Documentation of the pulmonary embolism is made most accurately with a pulmonary angiogram. The relatively invasive nature of this modality has accounted for reluctance to use the test, especially in frail, medically compromised patients. Other, less invasive modalities have supplanted pulmonary angiography for diagnosing a pulmonary embolism. Foremost is the ventilation-perfusion (/) scan, although the accuracy of this test is variable and depends on the experience of the reader. Spiral computed tomography (CT) and magnetic resonance imaging (MRI) have been reported as highly accurate, noninvasive alternatives to pulmonary angiography.

Management of Pulmonary Embolism There are three methods of managing pulmonary embolus. The first is heparin anticoagulation, which continues to be the most commonly used modality. Anticoagulation prevents propagation of thrombus and could prevent recurrent thromboembolism from the deep veins. It has never been shown to result in acceleration of clearance of the thrombus from the pulmonary vasculature. Patients with compromised right ventricular function on the basis of pulmonary artery obstruction continue to demonstrate echocardiographic changes long after the embolic event.

Thrombolytic therapy with intravenous urokinase or streptokinase, by contrast, results in the dissolution of pulmonary vascular thrombus and improvement in right ventricular function. The relatively small, randomized trials of the 1970s did not demonstrate mortality differences between patients treated with heparin versus thrombolysis, but their small size precluded a meaningful analysis of the endpoint of mortality. It is likely that thrombolytic therapy holds great potential to improve the clinical outcome of patients with pulmonary embolism, especially in those with sufficient thrombus burden to compromise right ventricular function. The cost of these benefits is a small but significant risk of distant bleeding complications.

Pulmonary embolectomy represents the third treatment modality for pulmonary embolism. It is indicated in patients with severe hemodynamic decompensation. The procedure carries a mortality of 50 percent when done through an open technique. A transvenous, percutaneous technique has been developed recently, and it holds potential as an isolated procedure or an adjunct to thrombolytic therapy (Fig. 21-1).

FIGURE 21-1 Algorithm for the management of pulmonary embolism. IVC = inferior vena cava; tPA = tissue plasminogen activator.


The prevalence of varicose veins increases with age and usually is greater in females. It is important to distinguish between primary varicose veins and varicosity secondary to underlying deep venous disease. Primary varicose veins may be inherited and are associated with incompetent valves within the superficial system alone. Secondary varicose veins occur as a result of incompetence in the communicating and deep veins of the leg. This results in high pressures within the superficial veins and subsequent dilatation and superficial venous incompetence. Complications are unlikely with primary varicose veins, but stasis dermatitis and ulceration frequently accompany secondary varicosities.

Patients with varicose veins are treated initially with conservative care, using compression stockings and limitation of prolonged standing. Injection sclerotherapy may be used if the veins are small or localized. Surgical excision is indicated when conservative measures fail. This frequently requires stripping of the greater saphenous vein in its entirety, including ligation of the adjoining branches in the groin. Accessory varicosities usually are excised through multiple small incisions.


Lower extremity edema occurs in three clinical settings: edema of fluid overload, venous insufficiency, and lymphedema. Lymphedema is unilateral or bilateral and is very slow to clear with elevation. The diagnosis of lymphedema frequently is based on clinical grounds. Management is supportive, with compression stockings and care taken to avoid factors that predispose the patient to cellulitis.

Lymphedema may be classified into primary and secondary varieties. The primary lymphedemas are classified as follows:

  1. Congenital: present at birth
  2. Praecox: onset in childhood
  3. Tarda: onset in adulthood

Lymphography has been useful in clarifying the primary lymphedemas into hyperplastic and hypoplastic varieties. Secondary lymphedema is frequently secondary to lymph node metastases and also may occur after radiation, trauma, surgical excision, or parasitic invasion.

Operative treatment is used rarely in patients with lymphedema. The attempts have been directed at removing the subcutaneous tissues of the extremity. The original procedure of Charles consisted of wide excision of the lymphedematous tissue followed by skin grafting of the extremity. Direct lympho-venous anastomoses have been undertaken at a few centers but have yet to be proved effective.

For a more detailed discussion, see Green RM, Ouriel K: Venous and Lymphatic Disease, chap. 21 in Principles of Surgery, 7th ed.

Copyright © 1998 McGraw-Hill
Seymour I. Schwartz
Principles of Surgery Companion Handbook

Principles of Surgery, Companion Handbook
Principles of Surgery, Companion Handbook
ISBN: 0070580855
EAN: 2147483647
Year: 1998
Pages: 277
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