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The anatomy of the veins and lymphatics provides the basis for understanding the pathophysiology of common disease states. With the primary purpose of the veins to return blood to the heart in a unidirectional fashion and for the lymphatics to carry excess interstitial fluid and particulate matter back to the central circulatory system, any interruption or alteration in normal flow patterns forms the basis for venous and lymphatic pathology.
The deep veins of the leg are bounded within their muscular compartments and enveloping fascia; they run together with the corresponding arterial and lymphatic structures. The anterior tibial, posterior tibial, and peroneal veins are generally paired and coalesce to form the popliteal vein or veins, which may also be paired. The popliteal vein passes superiorly through the adductor canal, becoming the femoral vein (previously referred to as the superficial femoral vein), which then merges with the deep femoral vein to form the common femoral vein. Cranial to the inguinal ligament, the common femoral vein becomes the external iliac vein. The external and internal iliac veins merge to form the common iliac vein. The left common iliac vein passes deep to the right common iliac artery and joins the right common iliac vein to become the inferior vena cava.
The superficial veins, lying above the muscular fascia, are bounded superficially by the saphenous fascia. The great saphenous vein originates at the level of the ankle and continues medially to the saphenofemoral junction, where it joins with the common femoral vein. Accessory saphenous tributaries arise from the saphenofemoral junction in variable anteromedial and anterolateral distributions ( Fig. 20.1 ). The small saphenous vein originates over the lateral ankle, lying above the muscular compartment, and is bounded by saphenous fascia superficially. It drains into the popliteal vein at the saphenopopliteal junction ( Fig. 20.2 ). Two anatomically important veins are the intersaphenous vein (often referred to as the vein of Giacomini), connecting the great and the small saphenous veins, and the posterior accessory great saphenous vein, draining the subcutaneous tissue and skin overlying the medial calf.
Perforating veins can be found along the length of the lower extremity, with the majority located below the knee. , These veins traverse the muscular fascia and connect the deep and superficial veins, with flow normally occurring from the superficial veins into the deep venous system. These perforators ( Fig. 20.3 ) are located from the level of the heel to the upper thigh along the medial leg in a narrow band and are often described based on named anatomic location or distance from the proximal medial malleolus.
The remaining veins lying above the muscular fascia and underneath the dermis are best described as communicating veins, which form a variable network that interconnects the named superficial veins.
Like those veins in the lower extremity, the deep veins of the upper extremity run in a paired fashion along with the radial and ulnar arteries, coalescing to form the brachial veins at the level of the antecubital fossa where they are bounded by the bicipital aponeurosis. Traversing the upper arm, the brachial vein or veins become the axillary vein or veins at the lower margin of the teres major muscle and subsequently the subclavian vein at the lateral edge of the first rib.
Superficial veins arising at the wrist include the cephalic and basilic veins, which lie above the muscular fascia underneath the skin and invariably become invested in superficial fascia at the level of the middle forearm. The cephalic vein continues along the lateral aspect of the arm, coursing to the level of the deltopectoral groove and finally joining the subclavian vein. Similarly, the basilic vein lies medially at the level of the wrist, beneath the skin, and courses to the level of the upper arm piercing the muscular fascia to join the brachial or axillary vein ( Fig. 20.4 ).
In the lower extremity the lymphatics can be divided into vessels and nodes. There are two sets of lymphatic vessels, which correspond to the deep and superficial veins. The vessels parallel the corresponding veins. There is a significantly increased number of superficial lymphatic vessels when compared with the deep lymphatic vessels. The vessels drain into lymphatic glands or lymph nodes. These are primarily found in the popliteal region, where it is common to see five to seven of them embedded within the popliteal fossa. In the inguinal region 10 to 20 nodes are present and are primarily found in the femoral triangle ( Fig. 20.5 ).
The lymphatic vessels of the upper extremity also follow the superficial and deep vascular structures. As in the lower extremity, the lymph node numbers increase moving proximally, with a significant number at the level of the axillary and supraclavicular region ( Fig. 20.6 ).
Most venous and lymphatic problems can be approached in an organized and sequential fashion. First, the presenting complaint should be determined; physical examination should correlate with the presenting history and should also provide a bridge to the pathophysiology of the disease process. When the history and physical examination have been completed, diagnostic studies can be ordered, if necessary, to further localize the disease or quantify the extent of the process. Therapy is ultimately driven by the natural history of the disease process and its impact on the patient’s quality of life as well as the patient’s risk factors and functional status. A relatively benign natural history, or significant and unmodified patient risk factors, may indicate an initial course of medical management, risk-factor modification, and observation; threat of significant hemodynamic consequences or tissue loss may indicate the need for a more aggressive intervention.
Typically, presenting symptoms can be broadly classified into the following categories: pain; weakness; neurosensory complaints including warmth, coolness, numbness, and hypersensitivity; discoloration; swelling; tissue loss and ulceration; and varicosities. The history should attempt to identify and characterize the location of the symptoms (unilateral, bilateral, proximal, distal); acuity of onset (sudden/gradual); duration; character, including frequency of symptoms and temporal patterns (continuous, intermittent); course or progression (better, worse, unchanged); and factors that aggravate and ameliorate the symptoms, including position, activity, temperature, menses, vibration, and pressure.
The physical examination should progress from observation and inspection to palpation. On observation, the extremity should be assessed for evidence of skin changes, including atrophy, cyanosis or mottling, pallor, rubor, lipodermatosclerosis, and ulcerations. The presence and location of edema should be identified and quantified by measurement of circumference. Tissue loss and ulceration should be noted and fully described, including the location, size and depth, as well as presence of associated cellulitis and inflammation. On initial palpation, changes in temperature and sensation should be noted and compared with the contralateral extremity. All accessible pulses should be evaluated. At a minimum, pulses should be classified as absent, decreased, or normal; with use of the Doppler when pulses are nonpalpable, especially in patients with marked edema, to confirm adequate arterial inflow.
The severity of venous diseases can be classified using multiple models that have been shown to be of value for clinical and research purposes. These include anatomic location ( Table 20.1 ; the Clinical, Etiologic, Anatomic, Pathophysiologic (CEAP) classification system ( Table 20.2 ); the Venous Clinical Severity Score (VCSS) ( Table 20.3 ); the Venous Segmental Disease Score (VSDS) ( Table 20.4 ); and the Venous Disability Score (VDS) ( Table 20.5 ). These various classification schemes are being increasingly used in clinical practice, and nationally for registry documentation. The Villalta ( Table 20.6 ), Ginsberg, Brandjes, Windmer, CEAP, and Venous Clinical Severity Score models were evaluated by Soosainathan et al., who concluded that the Villalta score, combined with a venous disease–specific quality-of-life measure were the preferred tools to characterize the post-thrombotic syndrome. Table 20.7 outlines available chronic venous disease–specific and health-related quality-of-life measures.
Number | Segment | ||
---|---|---|---|
Superficial veins (AS1–5) | |||
1 | Great saphenous vein | ||
2 | Above knee | ||
3 | Below knee | ||
4 | Small saphenous vein | ||
5 | Nonsaphenous | ||
Deep veins (AD6–16) | |||
6 | Inferior vena cava | ||
Iliac | |||
7 | Common | ||
8 | Internal | ||
9 | External | ||
10 | Pelvic: gonadal, broad ligament | ||
Femoral | |||
11 | Common | ||
12 | Deep | ||
13 | Superficial ∗ | ||
14 | Popliteal | ||
15 | Tibial (anterior, posterior, or peroneal) | ||
16 | Muscular (gastrocnemius, soleal, other) | ||
Perforating veins (AP17–18) | |||
17 | Thigh | ||
18 | Calf |
∗ The superficial femoral vein is now referred to as the femoral vein.
Category | Finding | Classification |
---|---|---|
Clinical | Asymptomatic | C0 |
Telangiectasias, reticular veins, malleolar flare | C1 | |
Varicose veins | C2 | |
Recurrent varicose veins | C2r | |
Edema, no skin changes | C3 | |
Changes in the skin and subcutaneous tissue secondary to CVD | C4 | |
Pigmentation or eczema | C4a | |
Lipodermatosclerosis and atrophie blanche | C4b | |
Corona phlebectatica | C4c | |
Skin changes as above with healed ulcer | C5 | |
Skin changes as above with active ulcer | C6 | |
Recurrent active venous ulcer | C6r | |
Etiologic | Primary | Ep |
Secondary | Es | |
Secondary – intravenous | Esi | |
Secondary – extravenous | Ese | |
Congenital | Ec | |
Anatomic | Superficial | As |
Reticular veins | As Ret | |
Great saphenous vein above knee | As GSVa | |
Great saphenous vein below knee | As GSVb | |
Small saphenous vein | As SSV | |
Anterior accessory vein | As AASV | |
Nonsaphenous vein | As NSV | |
Deep | Ad | |
Inferior vena cava | Ad IVC | |
Common iliac vein | Ad CIV | |
Internal iliac vein | Ad IIV | |
External iliac vein | Ad EIV | |
Pelvic veins | Ad PELV | |
Common femoral vein | Ad CFV | |
Femoral vein | Ad FV | |
Popliteal vein | Ad PV | |
Crural (tibial) vein | Ad TIBV | |
Peroneal vein | Ad PRV | |
Anterior tibial vein | Ad ATV | |
Posterior tibial vein | Ad PTV | |
Muscular veins | Ad MUSV | |
Gastrocnemius vein | Ad GAV | |
Soleal vein | Ad SOV | |
Perforator | Ap | |
Thigh perforator vein | Ap TPV | |
Calf perforator vein | Ap CPV | |
No venous anatomic location identified | An | |
Pathophysiologic | Reflux | Pr |
Obstruction | Po | |
Reflux and obstruction | Pro | |
No pathophysiology identified | Pn |
Attribute | Absent: 0 | Mild: 1 | Moderate: 2 | Severe: 3 |
---|---|---|---|---|
Pain | None | Occasional; not restricting activity or requiring analgesics | Daily; moderate activity limitation; occasional analgesics | Daily; severely limiting activities or requiring regular use of analgesics |
Varicose veins a | None | Few, scattered: branch varicose veins | Multiple: GS varicose veins confined to calf or thigh | Extensive: thigh and calf or GS and LS distribution |
Venous edema b | None | Evening ankle edema only | Afternoon edema above ankle | Morning edema above ankle and requiring activity change, elevation |
Skin pigmentation c | None or focal, low-intensity (tan) | Diffuse, but limited in area and old (brown) | Diffuse over most of gaiter distribution (lower ⅓ of leg) or recent pigmentation (purple) | Wider distribution (above lower ⅓ of leg) and recent pigmentation |
Inflammation | None | Mild cellulitis, limited to marginal area around ulcer | Moderate cellulitis, involving most of gaiter area (lower ⅓ of leg) | Severe cellulitis (lower ⅓ of leg and above) or significant venous eczema |
Induration | None | Focal, circummalleolar (<5 cm) | Medial or lateral, less than lower | Entire lower ⅓ of leg or more |
No. of acute ulcers | 0 | 1 | 2 | >2 |
Active ulceration | No | Yes; <3 months | Yes; >3 months, <1 year | Yes; not healed > 1 year duration |
Active ulcer, size | No | Yes; <2 cm | Yes; 2–6 cm | Yes; >6 cm (diameter) |
Compressive therapy | Not used or not compliant | Intermittent use of stockings | Patient wears elastic stockings most days | Full compliance: stockings and compliant elevation |
a “Varicose” veins must be >4 mm in diameter to qualify so that differentiation is ensured between C1 and C2 venous disease.
b Presumes venous origin from characteristics (e.g., brawny [not pitting or spongy] edema), with significant effect of standing/limb elevation and/or other clinical evidence of venous etiology (i.e., varicose veins, history of deep venous thrombosis). Edema must be regular finding (e.g., daily occurrence). Occasional or mild edema does not qualify.
Reflux b Score | Vein(s) | Obstruction b , c Score | Vein(s) |
---|---|---|---|
1/2 | Small saphenous | 0 d | |
1 | Great saphenous | 1 | Greater saphenous (only if thrombosed from groin to below knee) |
1/2 | Perforators, thigh | 0 d | |
1 | Perforator, calf | 0 d | |
2 | Calf veins, multiple (posterior tibial alone = 1) | 1 | Calf veins, multiple |
2 | Popliteal vein | 2 | Popliteal vein |
1 | Femoral vein | 1 | Femoral vein |
1 | Profunda femoris vein | 1 | Profunda femoris vein |
1 | Common femoral vein and above d | 2 | Common femoral |
1 | Iliac vein | ||
1 | Inferior vena cava | ||
10 | Maximum reflux score | 10 | Maximum obstruction score e |
a As determined by appropriate venous imaging (phlebography or duplex ultrasonography scan). Although some segments may not be routinely studied in some laboratories (e.g., profunda femoris and tibial veins), points cannot be awarded on the basis of presumption without scanning of the segments for obstruction or reflux.
b Reflux means that all the valves in that segment are incompetent. Obstruction means there is total occlusion at some point in the segment or >50% narrowing of at least half of the segment. Most segments are assigned 1 point, but some segments have been weighted more or less to fit with their perceived significance (e.g., increasing points for common femoral or popliteal obstruction and for popliteal and multiple calf vein reflux and decreasing points for lesser saphenous or thigh perforator reflux). Points can be assigned for both obstruction and reflux in the same segment; this is uncommon but can occur in some post-thrombotic states, potentially giving secondary venous insufficiency higher severity scores than primary disease.
c The excision, ligation, or traumatic obstruction of deep venous segments counts toward obstruction points just as much as their thrombosis.
d Normally there are no valves above the common femoral vein, so no reflux points are assigned to them. In addition, perforator interruption and saphenous ligation/excision do not count in the obstruction score, but as a reduction of the reflux score.
e Not all of the 11 segments can be involved in reflux or obstruction; 10 is the maximum score that can be assigned, and the maximum might be achieved by complete reflux at all segmental levels.
0 | Asymptomatic |
1 | Symptomatic but patient is able to carry out usual activities a without compressive therapy |
2 | Patient can carry out usual activities a only with compression and/or limb elevation |
3 | Patient is unable to carry out usual activities a even with compression and/or limb elevation |
a Usual activities = patient’s activities before onset of disability from venous disease.
Symptoms/clinical signs | None | Mild | Moderate | Severe |
---|---|---|---|---|
Symptoms | ||||
Pain | 0 points | 1 point | 2 points | 3 points |
Cramps | 0 points | 1 point | 2 points | 3 points |
Heaviness | 0 points | 1 point | 2 points | 3 points |
Paresthesia | 0 points | 1 point | 2 points | 3 points |
Pruritus | 0 points | 1 point | 2 points | 3 points |
Clinical signs | ||||
Pretibial edema | 0 points | 1 point | 2 points | 3 points |
Skin induration | 0 points | 1 point | 2 points | 3 points |
Hyperpigmentation | 0 points | 1 point | 2 points | 3 points |
Redness | 0 points | 1 point | 2 points | 3 points |
Venous ectasia | 0 points | 1 point | 2 points | 3 points |
Pain on calf compression | 0 points | 1 point | 2 points | 3 points |
Venous ulcer | Absent | Present |
Outcome Assessment | Focus on CVD | QoL Score a | Construct |
---|---|---|---|
SF-36 | Generic, applicable to a spectrum of nonvenous and venous diseases | Ascending | 36 items Physical and mental health 8 domains |
AVVQ – Aberdeen Varicose Vein Questionnaire | Varicose veins, CVD | Descending | 13 items Weighted scoring Patient draws varices onto template |
CIVIQ – Chronic Venous Insufficiency Questionnaire | General venous | Ascending | 20 items Diagnosis based on clinical and subjective symptoms; no objective confirmation of venous etiology |
VEINES – Venous Insufficiency Epidemiologic and Economic Study | General venous | Ascending | 35 items, 2 categories VEINES-Qol measures the effect on QoL VEINES-Sym measures symptoms |
CCVUQ – Charing Cross Venous Ulcer Questionnaire | Venous ulcer | Descending | 20 items Venous etiology confirmed with clinical examination and Duplex ultrasonography |
a Ascending scores indicate that a higher score means a better QoL, whereas a descending score indicates that a lower score has a better QoL.
Veins are normally patent and competent, with functioning valves. Pathologically, intraluminal thrombus can partially or completely obstruct a vein. Venous obstruction can remain asymptomatic, often associated with isolated tibial vein thrombosis, or can present with a symptomatic painful, swollen extremity. The latter is frequently associated with progression of the obstructing thrombus proximally. Untreated thrombosis, initially with minimal symptoms, can potentially lead to phlegmasia cerulea dolens and rarely limb loss.
Symptoms can be associated with compression, acute or chronic venous thrombosis, or postobstructive valvular incompetence and venous reflux. Isolated venous obstruction secondary to anatomic compression, such as that associated with May–Thurner syndrome, can result in mild to incapacitating swelling.
Patients with deep venous thrombosis (DVT) can present with varying symptoms and signs, depending on the extent of obstruction, the degree of inflammatory reaction, the location and anatomic extent of the obstruction, and associated comorbidities. DVT most commonly presents with unilateral swelling, discomfort, and a sense of fullness or pressure in the affected extremity. The symptoms are acute in onset and the pain is often characterized as an aching discomfort. There may be a sensation of tightness or heaviness. Patients will note that the symptoms are exacerbated with ambulation or when the legs are kept in a dependent position. Leg elevation, however, will often relieve the discomfort. Hospitalized patients with DVT can be asymptomatic, and approximately half of nonhospitalized patients presenting with classic symptoms suggestive of DVT will not have venous pathology.
In assessing the patient with suspected DVT, it is most important to determine any predisposing risk factors that may be present. Multiple risk factors can be associated with an increased threat of DVT, including advanced age; prolonged immobility, such as hospitalization or recent travel; recent surgery, pregnancy, significant trauma, cancer, a previous history of DVT, or a family history of venous thrombosis, and hypercoagulability such as seen in the recent COVID-19 pandemic (see Ch. 40 , Disorders of Coagulation: Hypercoagulable States). The presence or absence of risk factors can markedly influence the duration of treatment and the potential need for lifelong anticoagulation. ,
The differential diagnosis of DVT includes systemic causes of lower extremity swelling, which generally result in bilateral lower extremity edema. Congestive heart failure and cirrhosis (liver failure) are common systemic etiologies and may also be seen in patients with chronic renal insufficiency. The common denominator among systemic causes of lower extremity swelling is fluid overload or retention. The first manifestation of heart failure is progressive swelling of the legs, but it may also be associated with dyspnea and orthopnea.
Localized trauma or injury is most often associated with unilateral swelling. The differential diagnosis also includes cellulitis, muscle strain or tear, a Baker’s cyst, hematoma, or dermatitis. Although the diagnosis of DVT can be suspected based on the presence of pain, swelling, and associated risk factors, noninvasive imaging remains a necessary adjunct in order to confirm a suspected diagnosis.
In attempts to improve diagnostic accuracy in the patient with suspected DVT, various models for risk stratification have been developed since the signs and symptoms of DVT are often nonspecific. The most commonly used probability model is that of Wells ( Table 20.8 ) (see Ch. 148 , Acute Lower Extremity Deep Venous Thrombosis: Presentation, Diagnosis, and Medical Treatment). The Wells criteria include both subjective and objective elements, resulting in a score that indicates a low, moderate, or high risk of DVT. The Wells criteria have been prospectively validated and are in use clinically, especially in emergency departments, where routine use of vascular ultrasound is not practical and a low pretest probability is associated with only a 2% to 3% incidence of DVT. Unfortunately, the Wells scoring model still incorporates a subjective determination of alternative diagnoses, which, if present, significantly lower the clinical probability of DVT. Meta-analysis examining the clinical diagnosis of DVT suggests that the Wells criteria are most accurate in the identification of proximal DVT in cohorts of younger patients without a prior history of thromboembolism. Goodacre et al. examined 18 strategies used to diagnose suspected DVT. They concluded that the optimal strategy was to discharge patients with a low or intermediate Wells score and a negative D-dimer. Ultrasound was reserved for those patients with a high Wells score or a positive D-dimer. In a report by Neher et al., the authors reported that the accuracy of the D-dimer test varied with the method of analysis. The highest sensitivity was associated with the ELISA assay.
Clinical Feature | Score |
---|---|
Active cancer (treatment ongoing or within previous 6 months or palliative) | 1 |
Paralysis, paresis, or recent plaster immobilization of the lower extremities | 1 |
Recently bedridden >3 days or major surgery within 4 weeks | 1 |
Localized tenderness along the distribution of the deep venous system | 1 |
Entire leg swollen | 1 |
Calf swelling by more than 3 cm compared with the asymptomatic leg (measured 10 cm below tibial tuberosity) | 1 |
Pitting edema (greater in the symptomatic leg) | 1 |
Collateral superficial veins (nonvaricose) | 1 |
Alternative diagnosis as likely as or more likely than that of deep venous thrombosis | −2 |
The Caprini Risk Assessment model is specific to surgical patients, factoring in clinical variables based on a point system to determine a perioperative risk of DVT, and the appropriate perioperative prophylactic measures. This assessment has been validated to be accurate in appropriate populations ( Table 20.9 ). ,
Each risk factor = 1 point | Each risk factor = 2 points | Each risk factor = 3 points |
---|---|---|
|
|
|
For women only (1 point each) | Caprini risk category based on total risk score | Each risk factor = 5 points | |
---|---|---|---|
Total Score | Category | ||
|
0–4 | Low |
|
5–8 | Moderate | ||
≥9 | High |
Regardless of the presentation or physical findings, it is essential in the initial assessment of the patient presenting with DVT to determine the cause of the thrombotic event. This allows the provider to classify the event as either a “provoked” or “unprovoked” DVT. The duration of anticoagulation is markedly altered in those patients who present with an unprovoked DVT. They are by default considered potentially hypercoagulable, even in the presence of a negative laboratory workup, and consideration for lifelong anticoagulation should be entertained. The American College of Chest Physicians has provided ongoing evidence-based guidelines for the treatment of DVT. ,
DVT can also involve the subclavian and axillary veins in the upper extremity. Onset is typically acute and associated with swelling of the entire arm. There has always been a strong relationship between venous thrombosis and compression of the subclavian vein at the thoracic outlet due to abnormal rib, clavicle, and muscular pathology, and patients will frequently note an association with upper-body exercise and activity (see Ch. 126 , Thoracic Outlet Syndrome: Venous). More recently, subclavian and axillary vein thrombosis has been increasingly associated with subclavian vein catheters placed for central access (see Ch. 150, Acute Upper Extremity and Catheter-Related Venous Thrombosis).
The presence of any swelling or edema should be noted and described. Unilateral or bilateral involvement should be noted, as well as the extent of involvement (i.e., is the entire extremity swollen, or just the calf and foot?). Swelling associated with acute DVT is frequently unilateral. The entire extremity may be swollen in patients with iliofemoral venous thrombosis, while femoropopliteal venous obstruction frequently results in swelling of the calf or distal extremity. The left leg is more commonly affected. If there is unilateral swelling, it should also be determined if this results in a measurable discrepancy in the size of the leg relative to the contralateral extremity. In patients with unilateral swelling resulting in a difference in leg circumference of more than 3 cm, the potential for a deep venous thrombotic process is high. In contrast, absence of a significant change in limb circumference is associated with a very low likelihood of a DVT. Physical examination should also include the joints as well as other skin changes, as joint pain and localized cellulitis are rarely associated with DVT.
Homans sign describes the association between calf vein thrombus and calf pain with passive dorsiflexion of the foot. Other clinical findings that have been associated with acute DVT include the Bancroft sign, or tenderness on anteroposterior but not lateral compression of the calf, and the Lowenberg sign, which is calf pain associated with inflation of a blood pressure cuff about the calf. Unfortunately these “signs” persist in the literature and within medical documentation despite the fact that none of them are diagnostic of DVT.
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