Overview of Venous Disorders



Fig. 38.1
The main superficial veins of the lowerextremity



The principal return of blood flow of the lower extremities is through the deep veins. In the leg, the anterior tibial, posterior tibial, peroneal, and gastrocnemius veins join forming the popliteal vein at the popliteal fossa, ascending into the thigh, and becoming the femoral vein. In the groin, the femoral vein is joined by the deep femoral vein which enters the abdomen underneath the inguinal ligament becoming the external iliac vein [1].

The superficial venous system consists of two axial veins: the great saphenous vein (GSV) and the small saphenous vein (SSV) . Several epifascial veins connect the great saphenous vein and the small saphenous vein system. The posterior thigh circumflex vein, previously referred to as Giacomini’s vein, originates from the SSV or its thigh extension. It ends into the GSV or the posterior accessory vein [2, 3].

The great saphenous vein begins at the dorsum of the foot and ascends anterior to the medial malleolus at the ankle and anteromedial to the tibia. At the knee, the vein is in the medial aspect of the popliteal fossa and ascends in the anteromedial aspect of the thigh, joining the femoral vein in the groin through an opening of the superficial fascia called the fossa ovalis.

The saphenofemoral junction is a complex anatomic entity composed of one or several external pudendal veins, the superficial epigastric vein, the superficial circumflex vein, and one or several accessory saphenous veins, whose course in the leg can be anterior and posterior to the GSV [1]. The terminal valve and the preterminal valve are located at the saphenofemoral junction and a few millimeters distally (Fig. 38.2) [13].

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Fig. 38.2
(a, b) Schematic representation of the saphenofemoral junction . Note the configuration of the terminal valve (TV), preterminal valve (PTV), and suprasaphenic valve (SSV). From Caggiati A. et al. Nomenclature of the veins of the lower limb: extensions, refinements, and clinical application. J Vasc Surg. 2005. 41(4): 719–24. Reprinted with permission from Elsevier

Anatomic specimens and ultrasound technology have documented the GSV within a saphenous compartment , whose boundaries are the more superficial saphenous fascia and deeply by the muscular fascia of the limb (Fig. 38.3) [2, 3].

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Fig. 38.3
The saphenous compartment . MF muscular fascia, SL saphenous ligament. From Caggiati A. et al. Nomenclature of the veins of the lower limb: extensions, refinements, and clinical application. J Vasc Surg. 2005. 41(4): 719–24. Reprinted with permission from Elsevier

The small saphenous vein originates laterally from the dorsal venous arch of the foot and travels subcutaneously behind the lateral malleolus at the ankle. It ascends the calf in its own compartment between the heads of the gastrocnemius muscle to join the popliteal vein in the popliteal fossa [1]. Posterior and anterior accessory saphenous veins are present in the leg.

At several levels in the leg, and into the thigh, perforating veins connect the superficial and deep venous systems. The perforating veins are currently identified measuring the distance in centimeters from the heel. Names such as Hunterian, Dodd, and Cockett perforating veins are considered obsolete (Table 38.1) [2, 3].


Table 38.1
Perforating veins (PV) of the leg
























Gluteal perforators

Superior gluteal, midgluteal, lower gluteal PV

Thigh perforators

Medial thigh PV (formerly Hunter’s perforator) (PV of the femoral canal or inguinal PV)

Anterior thigh, lateral thigh PV

Posterior thigh PV (posteromedial, sciatic, posterolateral PV)

Pudendal PV

Knee perforators

Medial knee PV (formerly Boyd’s perforator)

Suprapatellar, lateral knee, infrapatellar, popliteal fossa PV

Leg (calf) perforators

Paratibial, posterior tibial PV (formerly Cockett’s perforators)

Anterior leg, lateral leg PV

Posterior leg PV (medial and lateral gastrocnemius, intergemellar, para-achillean PV)

Ankle perforators

Medial ankle, lateral ankle, anterior ankle PV

Foot perforators

Dorsal foot or intercapitular PV

Medial, lateral, plantar foot PV

The external iliac veins course in the pelvic retroperitoneal space, along the brim. Tributaries of the external iliac veins are the deep inferior epigastric, circumflex, and pubic veins. At the level of the sacroiliac joint, the external iliac veins join the internal veins forming the common iliac veins. The internal iliac veins drain from extrapelvic and intrapelvic tributaries. The common iliac veins of each side join into the inferior vena cava on the right side of the vertebral columns at the level of the fifth vertebral body. The right iliac artery crosses the origin of the left common iliac vein at the level of the fifth lumbar vertebral body. The inferior vena cava ascends on the right side of the spine and terminates in the right atrium. Tributaries are the lumbar, gonadal, renal, adrenal, inferior epiphrenic, and hepatic veins.

In the upper extremity, a superficial and deep venous system can be identified. Superficial veins of the upper extremity are the cephalic and basilic veins. The cephalic vein originates from the dorsal venous plexus on the radial side, while the basilic vein originates from the same plexus on the ulnar side. The cephalic vein ascends the lateral side of the arm and empties into the axillary vein through the infraclavicular fossa, perforating the clavipectoral fascia [4]. The basilic vein ascends the medial aspect of the arm and joins the axillary vein, after receiving the brachial vein. Several veins connect the cephalic and the basilic veins including the antecubital vein. The deep veins are the radial, ulnar, brachial, and axillary veins and are paired with the homonymous arteries.

At the lateral border of the first rib, the axillary vein becomes the subclavian vein [4]. At the medial border of the anterior scalene muscle, the subclavian vein forms the brachiocephalic vein with the internal jugular vein. Tributaries of the innominate vein are the vertebral, internal thoracic, and inferior thyroid veins. Behind the first right costal cartilage, the brachiocephalic veins from each side form the superior vena cava, whose course is to the right of the ascending aorta. Prior to entering the pericardium and emptying into the right atrium, the superior vena cava receives the azygos vein [4].

The azygos vein lies on the right side of the spine and originates at the level of the renal vein, sometimes as the cephalad extension of the ascending lumbar vein. Between the fourth and the sixth thoracic vertebrae, the azygos vein arches anteriorly, inferior to the right main bronchus, and empties into the superior vena cava. The hemiazygos has a similar origin but on the left side of the spine at the level of the eighth thoracic vertebra crosses the midline and empties into the azygos vein. The azygos and hemiazygos veins receive the subcostal and intercostal veins and anastomose with the paravertebral vein plexus [4].

The structure of the venous wall includes the intima, media, and adventitia. The intima enfolds forming bicuspid valves whose function is to assure venous return to the heart [4]. The dysfunction of venous valves is associated with acute and chronic venous disorders of the extremities.



Venous Disorders


Venous disorders can be divided into acute and chronic.


Acute Venous Disorders

Superficial

Deep

Chronic Venous Disorders

Primary

Telangiectasias

Reticular varicosities

Varicose veins

Secondary (post-thrombotic)

Venous obstruction

Chronic venous insufficiency (hyperpigmentation, lipodermatosclerosis, ulceration)


Acute Venous Disorders


Acute venous disorders are exclusively thrombotic. The physiology of the thrombotic event can be ascribed to Virchow’s triad: hypercoagulability, hemodynamic changes (venous stasis), and endothelial injury/dysfunction. Different manifestations of acute thrombosis are dictated by the affected venous bed. Examples are superficial thrombophlebitis, acute deep venous thrombosis, acute axillary-subclavian venous thrombosis, and portal vein system thrombosis.


Superficial Thrombophlebitis


Superficial thrombophlebitis is a common pathologic entity. It occurs in patients with lower extremity varicose veins, in association with malignancies (migratory thrombophlebitis), coagulopathies, and immune disorders/vasculitis, and is very commonly associated with catheters in patients receiving intravenous therapy [1].

Cardinal signs of a superficial thrombophlebitis are redness, heat, pain, and swelling, characterized by a linear, erythematous, tender, and swollen lesion along the course of a superficial vein [1]. The condition is self-limiting in the majority of patients, and as a result of the inflammatory reaction, the superficial vein becomes a palpable fibrotic cord.

Therapy includes removal of the intravenous catheter, nonsteroidal anti-inflammatory drugs (NSAIDs), compression therapy (a 20–30 mmHg compression stocking for the lower extremity), and extremity elevation.

The current recommendation from the American College of Chest Physicians antithrombotic guidelines suggests the administration of low molecular weight heparin at prophylactic dose for 4 weeks for patients with superficial vein thrombosis [5, 6]. If the thrombus ascends within 3 cm from the saphenofemoral junction, a 40% incidence of deep vein thrombosis with extension into the femoral vein has been observed. In this instance, full anticoagulation is recommended [5]. Recurrence and/or contraindications to anticoagulation may warrant a high ligation of the junction with excision of the affected GSV [5]. In a minority of patients, the thrombophlebitis can evolve into a suppurative infection requiring surgical resection of the infected vein and antibiotic therapy.


Acute Deep Vein Thrombosis


Recent data from the Centers for Disease Control and Prevention estimates that as many as 900,000 people (1–2 per 1000) are affected by deep vein thrombosis (DVT) and pulmonary embolism (PE) with estimates of 60,000–100,000 patients dying of the same cause in the United States [7]. Approximately 33% of the population with DVT/PE will develop a recurrence within 10 years, and one third of those patients will experience long-term complications such as post-thrombotic syndrome. Several risk factors that predispose to thrombosis, including thrombophilias, have been observed in the majority of patients with acute thrombotic events [7].


Risk Factors for Venous Thromboembolism

Age >40 years

Obesity

Trauma

Major abdominal surgery

Stroke/paraplegia

Congestive heart failure

Acute myocardial infarction

Malignancy

Oral contraceptives

Inflammatory bowel disease

Pregnancy


Thrombophilias

Coagulopathies

Antithrombin III deficiency

Protein C deficiency

Protein S deficiency

Activated protein C resistance

Factor V Leiden

Abnormal factor V cofactor activity

Dysfibrinogenemia

Hypoplasminogenemia

Hyperhomocysteinemia

Anticardiolipin antibody

Clinical signs of acute thrombosis of an extremity are swelling, pain, and discoloration. Occasionally, thrombosis of a major vein and its collaterals can cause worsening pain, edema, and cyanosis (phlegmasia cerulea dolens). Further progression may lead to a complete occlusion of the superficial venous system with impairment of the venous outflow and arterial circulation. The result is edema, pain, and paleness, followed by gangrene (phlegmasia alba dolens). This condition can be considered a medical and surgical emergency requiring prompt intervention. It is often associated with malignancy.

Pretest probability models, such as the Wells criteria , have been developed to facilitate the diagnosis of deep vein thrombosis. In conjunction with D-dimer testing, these models have been proven to safely rule out a DVT in outpatient settings [8].

Duplex ultrasound is the imaging modality of choice when pretest probability is intermediate to high [8]. Duplex ultrasound is highly sensitive and specific and shows noncompressibility of the affected vein. Adjuncts to the diagnosis are computed tomography (CT) venography and magnetic resonance (MR) venography that may further clarify the anatomy and thrombus cephalad extension (inferior vena cava and iliac veins).

The thrombosis of the left common iliac vein due to compression against the fifth lumbar and sacral vertebral bodies from the crossing right common iliac artery defines a condition called May-Thurner syndrome . It is seen in 20% of patients with left iliofemoral thrombosis. CT venogram and MR venogram (Fig. 38.4) are particularly useful in defining the syndrome [9]. May-Thurner syndrome may be associated with lower extremity edema and chronic venous insufficiency.

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Fig. 38.4
MR venogram of patient with May-Thurner syndrome . Note compression of the left common iliac vein from the right common iliac artery (Courtesy of Luigi Pascarella, University of Iowa Hospitals and Clinics)

The role of conventional venography is currently limited to a purely interventional intent [9]. Some authors advocate venography and intravascular ultrasound as an adjunct diagnostic modality [10].

The management of acute venous thrombosis has dramatically changed in the last decade. While anticoagulation has been considered the foundation for the treatment of these patients, more recently venography, catheter-directed thrombolysis (CDT), mechanical thrombectomy, and possible iliac vein stenting have shown benefit in patients with low bleeding risk. They have been shown to be effective in perithrombotic symptom control and in reducing the risk of post-thrombotic syndrome (PTS) [9, 11].

Post-thrombotic syndrome develops in 25–50% of patients with proximal lower extremity thrombosis. Its pathogenesis is complex and includes a post-thrombotic inflammatory reaction including the venous wall and valves with subsequent remodeling, development of venous hypertension, varicose veins, skin changes, and, ultimately, venous ulcers [1].

The results of the CaVenT (Catheter-directed Venous Thrombolysis in acute iliofemoral vein thrombosis ) study are consistent with a PTS absolute risk reduction of 14.4% (95% CI 0.2–27.9) with a number needed to treat of 7 (95% CI 4–502) at 24-month follow-up in the CDT group. This trend was confirmed at a 5-year follow-up with a 28% absolute risk reduction (95% CI 14–42) and a number needed to treat of 4 (95% CI 2–7) [11].

The CAVA (CAtheter Versus Anticoagulation alone for acute primary iliofemoral DVT ) and the ATTRACT (Acute Venous Thrombosis: Thrombus Removal with Adjunctive Catheter-Directed Thrombolysis ) trials are still ongoing, and results are yet to come [11].


Axillary-Subclavian Vein Thrombosis


Of particular interest is the spontaneous axillary-subclavian vein thrombosis associated with strenuous and repetitive activity of the upper extremities: the Paget-Schroetter syndrome (PSS) . It has been estimated that PSS accounts for 30–40% of acute axillary-subclavian vein thrombosis and 10–20% of upper extremity deep vein thrombosis [12].

This pathology is more prevalent in young individuals engaging in sporting activities with vigorous and sustained upper extremity motions, such as retroversion, hyperabduction, and hyperextension (e.g., wrestling, baseball, softball, tennis, gymnastics, cheerleading). In the majority of patients, the underlying anatomic abnormality is the partial compression of the axillary vein between the first rib and the clavicle due to a cervical rib, hypertrophy of the anterior and middle scalene muscles, and abnormal insertion of the scalene tendons. The narrowing of the costoclavicular angle and the persistent and sustained injury to the venous parenchyma cause the abrupt thrombosis [1, 12].

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Dec 8, 2017 | Posted by in CARDIOLOGY | Comments Off on Overview of Venous Disorders

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