Which veins are considered deep

Following the common femoral vein, it bifurcates into the deep femoral vein and the femoral vein Fig. In the more distal part of the medial thigh, only the femoral vein is visible Fig. When the transducer approaches the popliteal fossa of the posterior knee, the popliteal vein is visible.

The popliteal vein is superficial to the popliteal artery at the posterior knee Fig. Duplicated femoral veins or popliteal veins can be seen [ 13 ].

Because a duplicated venous segment may result in false-negative results, both lumens should be carefully examined Supplementary Fig. Manual vein compression is recommended every cm [ 3 ]. When tracing the popliteal vein downward, two posteriorly branching veins are found in the calf from the posteromedial approach. The vein along the tibia is the posterior tibial vein, and the vein along the posteromedial aspect of the fibula is the peroneal vein.

In a US approach, the cortical shadow of the tibia and fibula can be used as a bony landmark. The paired veins are present on both sides of the artery Fig. Just above the echogenic interosseous membrane between the tibia and the fibula, the anterior tibial artery and vein can be found.

If the posterior tibial vein cannot be traced in the proximal to distal direction, it is helpful to trace the vein upward from the posterior to the medial malleolus, where this vein is located more superficially. If the popliteal and calf veins are not visualized well in the supine-based position, the prone or decubitus position can also be helpful.

The distal femoral vein at the level of the adductor hiatus can be difficult to evaluate because of its depth and the transducer location. Above the interosseous membrane arrowheads between the tibia T and the fibula F , the anterior tibial vein arrows and artery open arrows are visible.

The sonic window is demonstrated through computed tomography venography. The two major superficial veins of the lower extremities are the great saphenous vein GSV and small saphenous vein SSV. The GSV begins in the medial marginal vein of the dorsum of the foot, ascends anteriorly to the medial malleolus, and passes posteromedially to the knee. The vein then ascends medially in the thigh to perforate the muscular fascia and join the common femoral vein at the saphenofemoral junction, a few centimeters distal to the inguinal ligament.

Tributaries of the GSV are variable between individuals, but there are general rules for naming them [ 10 ]. When the tributary courses obliquely, it is called the circumflex vein the posterior thigh circumflex vein or the anterior calf circumflex vein Fig. However, despite attempts to standardize the terminology, various terms have been used and many of the tributaries are difficult to name.

The great saphenous vein GSV arises from the medial aspect of the dorsal pedal venous arch, ascends anteriorly to the medial malleolus, passes posteromedially to the knee, and ascends medially in the thigh to join the common femoral vein through the saphenofemoral junction.

Tributaries of the GSV are named according to their course. A tributary that courses obliquely is called a circumflex vein.

The small saphenous vein SSV arises from the dorsal pedal arch and ascends along the middle of the calf and ends in the popliteal vein through the saphenopopliteal junction SPJ.

Before it penetrates the muscular fascia, the SSV may branch out a cranial extension, known as the vein of Giacomini, which goes upward to join the GSV. The SSV arises from the dorsal pedal arch and ascends posterolaterally from behind the lateral malleolus. It ascends along the middle of the calf and ends in the popliteal vein in the posterior knee. However, there are many variations in the termination of the SSV, including without connection to the popliteal vein [ 5 , 14 ].

Before it penetrates the muscular fascia, it may branch out a cranial extension that goes upward to join the GSV through the posterior thigh circumflex vein the vein of Giacomini Fig. Insufficiency of the superficial veins should be evaluated with the subject in the erect position, as the supine position may underestimate or miss the reflux of the venous flow Fig.

The reverse Trendelenburg position can be used if an erect position is impossible. The examined leg should be in a non-weightbearing position [ 1 ]. The saphenofemoral junction is visible on the anteromedial surface of the common femoral vein in the transverse view. A longitudinal view of the saphenofemoral junction Fig.

Normally, the terminal valve at the saphenofemoral junction prevents backward flow into the GSV. After a provocation test, such as the Valsalva maneuver, retrograde flow in the proximal GSV persisting for more than 0. Patient position standing and schematic representation of the transducer locations are shown here. Longitudinal view of the saphenofemoral junction and the corresponding sonic window in computed tomography venography based on transducer location are demonstrated.

In most cases, a terminal valve arrows near the saphenofemoral junction prevents backward flow into the great saphenous vein. CFV, common femoral vein. Examination of the GSV shows the echogenic fascia surrounding the GSV, which is bordered deeply by the muscular fascia arrows and superficially by the saphenous fascia arrowheads. Transverse ultrasonography examination at the level of the knee shows the saphenous compartment arrowheads overlying the tibia T and the muscle fascia of the medial gastrocnemius G.

There is an echogenic fascia surrounding the GSV that is bordered deeply by the muscular fascia and superficially by the saphenous fascia. The saphenous compartment is also visible at the knee level, above the tibia and medial gastrocnemius Fig. Unfortunately, however, there are many variations in the relationship of the fascial compartment to the GSV. Sometimes there is a large tributary outside of the saphenous compartment, while the distal GSV is hypoplastic or even absent [ 14 , 16 ].

The SSV is visible at the middle of the gastrocnemius belly in the fascial trunk Fig. In tracing the SSV upward, it enters into the popliteal vein. The longitudinal view of the saphenopopliteal junction, like the saphenofemoral junction of the GSV, is useful for assessing insufficiency of the SSV.

In the saphenopopliteal junction, calf squeezing augments the venous flow at first, followed by retrograde flow. As described above, however, there are many anatomical variations in this region, and the saphenopopliteal junction may be absent or rudimentary [ 5 , 14 ]. Patient position and schematic representation of the transducer locations are shown here. In the transverse view of the posterior calf, the SSV is seen in the middle of the gastrocnemius G belly in the fascial trunk arrowheads.

Longitudinal ultrasound view and the corresponding sonic window in computed tomography venography based on transducer location are demonstrated. However, many variations are noted in this region, and the saphenopopliteal junction can be absent or hypoplastic. The perforating veins connect the deep veins with the superficial veins and direct the flow from the superficial to the deep system. There are numerous perforators in the leg. According to a consensus statement [ 10 ], perforators are named after their locations.

Major groups classify perforators according to their longitudinal location as ankle, leg, knee, and thigh perforators. Subgroups indicate side i. Thus, the complete name of the perforator is a combination of the level and side i. More detailed subgroups are present for medial thigh and medial leg perforators. The medial thigh perforators are further classified as the perforating vein of the femoral canal and inguinal perforating vein, and the medial leg perforators are subdivided into the paratibial and posterior tibial perforating veins Fig.

This is convenient becausez it eliminates eponyms such as Hunterian, Dodd, Boyd or Cockett, all of which have been used commonly, but are confusing. The medial thigh perforator includes the PV of the femoral canal and the inguinal PV. Normally, the perforating veins are not clearly visible on US. Lack of regular physical activity can often affect both superficial and deep vein health. If you have concerns about your risk for superficial or deep vein thrombosis, please visit us here to schedule an appointment with one of our board-certified specialists at VeinSolutions in Austin, or contact us at VEIN For VeinSolutions in Georgetown, please contact us at February is American Heart Month.

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It is mandatory to procure user consent prior to running these cookies on your website. Patient Portal. October 26, What is the difference between superficial and deep veins? Treatment of lower and upper extremity DVT is generally the same. General supportive measures include pain control with analgesics, which may include short 3- to 5-day courses of a nonsteroidal anti-inflammatory drug NSAID.

Extended treatment with NSAIDs and aspirin should be avoided because their antiplatelet effects may increase the risk of bleeding complications. In addition, elevation of legs supported by a pillow or other soft surface to avoid venous compression is recommended during periods of inactivity. Patients may be as physically active as they can tolerate; there is no evidence that early activity increases risk of clot dislodgement and PE and may help to reduce the risk of the postphlebitic syndrome 1 Treatment reference Deep venous thrombosis DVT is clotting of blood in a deep vein of an extremity usually calf or thigh or the pelvis.

For details on drugs and their complications, see Drugs for Deep Venous Thrombosis Drugs for Deep Venous Thrombosis All patients with deep venous thrombosis DVT are given anticoagulants and in rare cases thrombolytics. A number of anticoagulants are effective for management of deep venous thrombosis see All patients with DVT are given anticoagulants.

Typically, patients are initially given an injectable heparin unfractionated or low molecular weight for 5 to 7 days, followed by longer term treatment with an oral drug. For patients who are to start warfarin , warfarin is started within 24 to 48 hours after the start of the injectable heparin. For patients who are to start an oral factor Xa inhibitor edoxaban or dabigatran etexilate , the oral agent is started on the day after the 5 to 7 days of injectable heparin is completed.

The reason for this different approach is that when starting warfarin , it takes about 5 days to attain a therapeutic effect; hence, the need to overlap with rapidly acting heparin for 5 to 7 days. On the other hand, oral factor Xa inhibitors and dabigatran attain a therapeutic effect within 2 to 3 hours of intake and there is no need to overlap these drugs with an injectable heparin. Select patients may continue treatment with a low-molecular-weight heparin rather than switching to an oral drug, eg, patients with extensive iliofemoral DVT or selected patients with cancer.

Alternatively, anticoagulation may be initiated with selected direct oral anticoagulants rivaroxaban or apixaban without first giving an injectable heparin ; however, use of these drugs may be limited due to higher cost compared to warfarin. Inadequate anticoagulation in the first 24 to 48 hours may increase risk of recurrence or PE. Acute DVT can be treated on an outpatient basis unless severe symptoms require parenteral analgesics, other disorders preclude safe outpatient discharge, or other factors eg, functional, socioeconomic might prevent the patient from adhering to prescribed treatments.

An IVC filter may help prevent pulmonary embolism in patients with lower extremity DVT who have contraindications to anticoagulant therapy or in patients with recurrent DVT or emboli despite adequate anticoagulation.

An IVC filter is placed in the inferior vena cava just below the renal veins via catheterization of an internal jugular or femoral vein. Some IVC filters are removable and can be used temporarily eg, until contraindications to anticoagulation subside or resolve. IVC filters reduce risk of acute embolic complications but can have longer-term complications venous collaterals can develop, providing a pathway for emboli to circumvent the filter, and there is also an increased risk of recurrent DVT.

Also, IVC filters can dislodge or become obstructed by a clot. A clotted filter may cause bilateral lower extremity venous congestion including acute phlegmasia cerulea dolens , lower body ischemia, and acute kidney injury Acute Kidney Injury AKI Acute kidney injury is a rapid decrease in renal function over days to weeks, causing an accumulation of nitrogenous products in the blood azotemia with or without reduction in amount of urine Treatment for a dislodged filter is removal, using angiographic or, if necessary, surgical methods.

IVC filters should be removed whenever possible. Thrombolytic drugs, which include alteplase , tenecteplase , and streptokinase, lyse clots and may be more effective than anticoagulation alone in selected patients, but the risk of bleeding is higher than with heparin. Consequently, thrombolytics should be considered only in highly selected patients with DVT. Patients who may benefit from thrombolytics include those Surgery is rarely needed.

However, thrombectomy, fasciotomy, or both are mandatory for phlegmasia alba dolens or phlegmasia cerulea dolens unresponsive to thrombolytics to try to prevent limb-threatening gangrene.

Chest —, It is preferable and safer to prevent DVT than to treat it, particularly in high-risk patients. DVT prophylaxis begins with risk assessment. Risk, along with other factors Anticoagulation eg, low molecular weight heparin , fondaparinux , adjusted-dose warfarin , direct oral anticoagulant.

IVC filters are sometimes used in situations where efficacy is not proven, for example, for the primary prevention of PE in patients after certain types of surgery or in patients with multiple severe injuries. Symptoms and signs are nonspecific, so clinicians must be alert, particularly in high-risk patients. Low-risk patients may have D-dimer testing, as a normal result essentially excludes deep venous thrombosis DVT ; others should have ultrasonography. Treatment initially is with an injectable heparin unfractionated or low molecular weight heparin [LMWH] followed by an oral anticoagulant warfarin , dabigatran, or a factor Xa inhibitor or perhaps a LMWH; alternatively, the oral factor Xa inhibitors rivaroxaban and apixaban may be used for initial and ongoing treatment.

Duration of treatment is typically 3 or 6 months, depending on the presence and nature of risk factors; certain patients require lifelong treatment. Early mobilization, leg elevation, and an anticoagulant are the recommended preventive measures; patients who should not receive anticoagulants may benefit from intermittent pneumatic compression devices, elastic stockings, or both. From developing new therapies that treat and prevent disease to helping people in need, we are committed to improving health and well-being around the world.

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