Subclavian Vein Thrombosis

Background

Sir James Paget first described thrombosis of the subclavian veins in 1875.[1] He coined the name gouty phlebitis to describe the spontaneous thrombosis of the veins draining the upper extremity. He observed that the syndrome was accompanied by pain and swelling of the affected extremity. However, he incorrectly attributed the syndrome to vasospasm. In 1884, von Schrötter postulated that this syndrome resulted from occlusive thrombosis of the subclavian and axillary veins.[2] In recognition of the work of these pioneers, in 1949, Hughes coined the term Paget-von Schrötter syndrome.[3] A related condition is thrombosis of the subclavian vein that is induced by the presence of indwelling catheters. The incidence of this condition has increased remarkably over the past two decades because of the extensive use of catheters in patients with cancer and other chronic medical conditions.

See the images below.

This figure shows the area where the subclavian vein is obstructed in the neck area. The vein is usually compressed by the first rib, clavicle, and serratus anterior muscle. A venogram in a patient with subclavian vein obstruction. Long-standing obstruction causes development of collaterals. Recanalization after thrombolytic therapy and stent placement. Patient underwent first rib resection and scalenectomy later. NextHistory of the Procedure

Patients may describe a history of trauma or, more frequently, strenuous use of the arm (>50% of cases). Common precipitating activities involve repeated hyperabduction and external rotation of the arm or backward and downward rotation of the shoulder. Causative activities may include participating in cricket, tennis, wrestling, lifting weights, water polo, gymnastics, baseball, or chopping wood. Because the symptoms of subclavian stenosis are fairly dramatic, most patients present promptly to the emergency department, usually within 24 hours. They may report dull ache in the shoulder or axilla, and the pain often is worsened by activity. Conversely, rest and elevation often relieve the pain. Patients with catheter-associated axillary subclavian deep vein thrombosis (ASDVT) report similar symptoms of the ipsilateral arm or shoulder with the indwelling catheter.

PreviousNextEpidemiologyFrequency

Prior to 1967, thrombosis of the axillary or subclavian vein accounted for 1-2% of all cases of deep vein thrombosis. Since then, the incidence has risen due to the more frequent use of central venous access for multiple clinical conditions. Among patients with effort-induced thrombosis with subclavian vein stenosis, the thrombosis occurs in the dominant arm in 80% of cases.

PreviousNextEtiology

The primary etiology is referred to as effort-induced thrombosis or Paget-von Schrötter syndrome. It usually results from the excessive use of the involved arm by predisposed individuals.

The secondary etiology is subclavian vein catheterization, especially in patients with cancer. (For detailed descriptions of catheterization techniques, see Central Venous Access, Subclavian Vein, Subclavian Approach and Central Venous Access, Subclavian Vein, Supraclavicular Approach.) Other causes include transvenous pacemakers, factor V Leiden mutation, protein C deficiency, protein S deficiency, antithrombin III deficiency, and prothrombin 20210A mutation. Long-term parenteral nutrition and use of hemodialysis catheters account for some cases of subclavian vein thrombosis.[4] Trauma is only rarely associated with this syndrome.

In a few cases, the diagnosis remains unknown. However, routine follow-up with these patients has revealed the development of lung cancer within 1 year of follow-up. The most common lung malignancy associated with subclavian thrombosis has been the Pancoast tumor.

PreviousNextPathophysiology

During long term venous catheterization of the subclavian and internal jugular vein in cancer patients, the risk of complications appear to be similar. However, for short term catheterization, subclavian vein catheterization is recommended because of the decreased risks of thrombotic complications and catheter colonization by skin flora. For patients requiring hemodialysis, both the femoral and internal jugular veins appear to have similar thrombotic complications. However, the risk of mechanical complications via the internal jugular vein appear to be higher. The subclavian vein should be avoided for both long and short term hemodialysis as the risk of thrombosis is very high.[5]

Differentiating catheter-associated subclavian vein thrombosis and Paget-von Schrötter syndrome is important because they appear to have different natural histories.

Paget-von Schrötter syndrome

It sometimes is referred to as spontaneous axilla-subclavian vein thrombosis to express the usually dramatic unexpected presentation of the disorder in otherwise healthy, generally young individuals. Over the past 2 decades, recognition has grown that the disorder can occur equally in both sexes and can affect all age groups. In the 1960s, the term effort-induced thrombosis was used to describe this disease to acknowledge that it often follows unusually strenuous use of the arm or shoulder on the affected side.

The pathophysiology of effort-induced thrombosis is multifactorial. It involves compressive changes in the vessel wall, stasis of blood, and hypercoagulability. External compression of the axillary-subclavian vein has been suggested to contribute to the stasis of blood that engenders thrombosis.

The factors that cause external compression include (1) anomalous subclavius or anterior scalene muscle, long transverse process of cervical spine, cervical rib, abnormal insertion of the first rib, congenital fibromuscular bands, or narrowing of the costoclavicular space from depression of the shoulder; (2) stress from exercise temporarily causing hypercoagulability; and (3) repetitive shoulder-arm motion causing microscopic intimal tears in the vessel wall. These factors, taken together, satisfy the classic Virchow triad for thrombosis. Furthermore, coexistent hematologic abnormalities that can contribute to thrombosis include protein C deficiency, antithrombin III deficiency, factor V Leiden mutation, and prothrombin 20210A mutation.

Catheter-induced subclavian vein thrombosis

Introducing catheters and transvenous pacemakers in to the subclavian vein alters the venous flow and increases turbulence. This results in platelet aggregation, release of procoagulants, and, ultimately, fibrin deposition. This causes a further reduction in the lumen of the vessel due to thrombus formation, which eventually culminates in total vessel occlusion. Intravenous medications and even parenteral nutrition have been known to cause thrombophlebitis. In patients with cancer, an additional contributing factor is that the tumor may generate procoagulant factors, predisposing to thrombosis at sites remote from the tumor.

PreviousNextPresentation

Not all patients with subclavian vein thrombosis are symptomatic. Those with symptoms may present with mild-to-moderate nonpitting edema and mild cyanosis of the hands and fingers on the affected side. Dilatation of subcutaneous collateral veins may be present over the upper arm and chest. This later sign may be the only clue to ASDVT in otherwise asymptomatic patients with catheter-related venous thrombosis. In a few cases, in which the diagnosis was missed or delayed or the patient presented late, the thrombus may have extended to the superior vena cava. These patients show most features of the superior vena cava syndrome, including face and neck swelling, periorbital edema, blurred vision, and some degree of facial cyanosis.[6]

PreviousNextIndications

In patients with effort-induced vein thrombosis of less than 2 weeks duration, thrombolytic therapy is recommended. Chronic ASDVT does not respond to thrombolytics and is better treated either conservatively with warfarin, or by surgical bypass, if symptoms are severe.

PreviousNextRelevant Anatomy

The subclavian vein courses over the first rib and posterior to the clavicle. The artery lies superior and posterior to the vein.

PreviousNextContraindications

Surgery is rarely indicated in ASDVT associated with central lines. Thrombolytic drug therapy is rarely recommended for patients who present with chronic subclavian vein thrombosis.

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Subclavian Artery Thrombosis

Background

Subclavian artery thrombosis is a condition in which the blood flow through the vessel is obstructed. The condition usually occurs secondary to some form of antecedent injury to the vessel, hypercoagulable state, or atherosclerotic changes. The condition is common in young athletic individuals who exert a significant amount of upper body activity.[1] Sudden occlusion from emboli followed by thrombosis of the artery is common in the population with signs of significant atherosclerotic disease.

The patient presenting with acute subclavian artery occlusion usually has a history of repetitive use and/or stress injury to the upper extremity on the affected side. A history of upper extremity claudication is common.

In situations in which the occlusion is secondary to atherosclerosis, acute thromboses of the artery are generally asymptomatic. In fact, in 9% of autopsy series, the left subclavian artery was either stenotic or occluded. If symptoms are present, upper extremity claudication on the affected side is most common. The patient may also present with dizziness, vertigo, imbalance, visual disturbances, or hemisensory dysfunction indicative of a subclavian steal syndrome. However, note that subclavian steal is observed on 2% of cerebral angiograms and causes no symptoms.

NextProblem

The occlusion arises secondary to damage to the intima of the artery. This damage can occur as a result of external muscular compression and repetitive stress to the artery or because of atherosclerotic changes to the vessel. Embolic phenomena and hypercoagulable states are also contributing factors.

Symptoms occur secondary to lack of blood flow to the affected extremity. To maintain blood supply to the extremity, blood is naturally rerouted from the vertebral, carotid, and internal mammary arteries, producing the various steal syndromes.

PreviousNextEpidemiologyFrequency

Symptomatic lesions occur in less than 1% of the population. In autopsy series, 9% of the population demonstrate stenosis or occlusion of one subclavian artery, usually on the left. Two percent of cerebral angiograms demonstrate asymptomatic subclavian steal.

PreviousNextEtiology

The occlusion arises secondary to damage to the intima of the artery. This damage can occur as a result of external muscular compression and repetitive stress to the artery, atherosclerotic changes to the vessel, or inflammatory processes.

Embolic or thrombotic occlusion of the artery occurs, particularly in the presence of atherosclerotic stenoses. Hypercoagulable states contribute to this scenario.

PreviousNextPathophysiology

The affected artery demonstrates detectable intimal damage, which is usually secondary to compressive forces exerted by the muscles of the shoulder girdle that compress the artery. Bony abnormalities in this area can also contribute to the process.[2] As these muscles enlarge secondary to physical activity, they exert pressure on the artery. This pressure, coupled with exertional activity of the upper extremity, can stretch and compress the intima, thus disrupting its natural integrity. This disruption precipitates platelet deposition in the area, with resulting thrombosis.

Atherosclerotic changes in the vessel occur secondary to the flow characteristics in the area. These depositions are accelerated by all of the dietary and sociological influences that affect the progression of atherosclerotic disease, including smoking, hypercholesterolemia, and hypertension. Occlusion secondary to atherosclerosis is more insidious and often causes no symptoms. At times, the symptom complex of claudication precedes the actual loss of blood flow.

Patients with hypercoagulable states, either intrinsic or secondary to dehydration complicated by concomitant cardiac arrhythmias and systemic inflammatory processes, comprise a small subset of individuals who may exhibit this pathology.

PreviousNextPresentation

A patient with an acute occlusion presents with a cold, painful, pulseless upper extremity. Axillary, brachial, and radial pulses are generally absent. When the occlusion is secondary to atherosclerotic changes, various prodromes and manifestations may be observed.

The patient may present with no symptoms or upper extremity claudication secondary to exertion. If the condition has precipitated a steal syndrome, no symptoms are typically present. The examining physician should be aware of the rare presentation of various neurological symptoms and findings that may be associated with the steal syndromes, including syncope, vertigo, ataxia, sensory loss, visual changes, and stroke, depending on the vessels involved in the steal. The affected upper extremity may or may not demonstrate diminished pulses. Blood pressure differences between the affected and unaffected sides may be noted.

PreviousNextIndications

Therapeutic intervention is indicated in any symptomatic patient once the etiology of the symptoms has been defined. For instances of upper extremity claudication or acute thrombosis in which the problem has been attributed to the subclavian artery, intervention should be planned and executed. For patients in whom cerebrovascular symptoms predominate, a careful neurological evaluation must be undertaken in order to isolate the problem. Once the anatomical aberration has been defined, intervention is indicated if the subclavian artery is involved.

PreviousNextRelevant Anatomy

In patients with subclavian artery occlusion secondary to variations in the thoracic outlet, 2 areas can undergo vascular compression during hyperabduction of the extremity. One site is where the axillary artery passes posterior to the pectoralis minor muscle and beneath the coracoid process. The other point is where the artery courses between the clavicle and the first rib. Fibrous tissue proliferation in this area can impose extrinsic compression on the vessel. The image below illustrates the relevant anatomy.

The anatomy of the subclavian artery in the thoracic outlet.

Aberrant origins of the subclavian artery off the aortic arch can be a cause of subclavian artery occlusion.[3]

In atherosclerotic disease, the carotid-subclavian junction or carotid-vertebral junctions are areas that appear to be predisposed to atheromata formation and calcification. Subsequently, this region is most likely to be involved in the occlusive process.[4]

Areas of the subclavian artery that are exposed to repeated forms of injury resulting in intimal damage are predisposed to occlusion.

PreviousNextContraindications

Contraindications to surgical intervention include inadequate distal runoff, inadequate vessel size, and marked collateralization of the occluded area. Concomitant medical problems that would endanger the patient during a surgical intervention are also contraindications to surgery. With the advent of stenting, patients with greater medical challenges can be treated successfully; however, the presence of appropriate arterial runoff and adequate artery size are imperative in order to ensure success of the procedure.

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Bedside Ultrasonography in Deep Vein Thrombosis

OverviewIntroduction

Venous thrombosis is a major cause of morbidity and mortality in the United States and a frequent cause of presentation in many emergency departments (EDs). The sequelae of deep vein thromboses (DVTs) range from the more common chronic venous stasis to the most serious pulmonary emboli (PEs).[1] PEs have been described as one of the most common preventable causes of death, and approximately two thirds of PEs are estimated to originate in the lower extremities as DVTs. The rate of propagation from DVT to PE is estimated to range from 10-50%.[2, 3, 4] Treatments with anticoagulation or Greenfield filter placement are extremely effective if used early, thereby underscoring the need for rapid diagnosis.

Compression ultrasonography has proven to be a highly sensitive and specific modality for the recognition of lower extremity DVTs without the need for radiation or contrast exposure.[5, 6] Traditional lower extremity studies interrogate and review the entire lower extremity vasculature, are performed by an ultrasonography technologist, and are read by a radiologist.[7, 8] However, these factors are not always available and have been shown to delay the time to diagnosis and potential treatment of a DVT by up to 2 hours.[9, 10]

To detect proximal lower-extremity DVTS, EDs now use a modified 2-point compression technique that focuses on the highest probability areas, decreases the study time to less than 5 minutes, and provides similar sensitivity and specificity.[11, 12, 13] In patients with a clinically suspected DVT, a negative compression ultrasound study may safely delay the need for anticoagulation therapy.[14] The 2-point DVT compression examination has been assessed in multiple randomized controlled studies and is well accepted when used properly with pretest probability assessments.[11, 15, 16]

The safety, ease of use, rapid time to diagnosis, low cost, and accessibility make bedside ultrasonography for DVT especially useful for emergency and critical care clinicians.

Indications

Patients who have risk factors for DVT or pulmonary embolism (PE), and in whom a clinician suspects DVT or PE, should have workups that include, but are not necessarily limited to, bedside compression ultrasonography.

Contraindications

No absolute contraindications to bedside ultrasonography for DVT exist.

If the clinical suspicion and pretest probability for a PE are high enough that a spiral computed tomography (CT) scan with intravenous contrast or V/Q (ventilation/perfusion) scan is warranted, then ultrasonography should not delay such studies or any further treatment goals. Additionally, thrombus in the pelvic veins will not be detected with this technique and, although rare, may be best evaluated with CT or magnetic resonance (MR) venography.[17]

NextPreparationEquipment

The following equipment is indicated:

Portable bedside ultrasound machine with a high-resolution linear transducerUltrasound gelPositioning

The patient should be supine with the leg in question exposed up to the inguinal ligament. Bedside ultrasonography for deep vein thrombosis (DVT) is performed in 2 principal positions, one for each area of examination. The images below depict ideal positions. Patient status and cooperation, however, ultimately determine what kind of positioning is possible. Ideally, 30-40 degrees of reverse Trendelenburg facilitates the examination by increasing venous distention.

When examining the femoral vein, the patient should be supine with the hip externally rotated and flexed, as shown below.

Patient positioning when assessing the femoral vein.

When examining the popliteal vein, the patient needs to expose the popliteal fossa on the posteromedial aspect of the knee. The patient can either dangle the leg off the edge of the bed or bend the knee and externally rotate the hip, as shown below. If necessary, the patient can also be rolled onto his or her side or into the prone position.

Patient positioning when assessing the popliteal vein. PreviousNextTechniqueOverview

Set up the portable ultrasound machine at the patient's bedside, with the linear transducer set at a frequency of 5.0-7.0 MHz. Expose the patient’s entire leg.

By convention, clinicians in EDs scan in an abdominal orientation with the probe marker pointed toward the patient’s head or right side. During the bedside ultrasonographic examination for deep vein thrombosis (DVT), the technician maintains this convention; that is, the probe marker points toward the patient’s right. In terms of orientation, remember that the top of the viewing screen is always where the transducer is touching the patient. Vascular anatomy is shown in the image below.

Lower extremity vascular anatomy.

The video below demonstrates ultrasonographic evaluation for DVT.

Demonstration of leg evaluation for deep vein thrombosis (DVT). Video courtesy of Meghan Kelly Herbst, MD. Also courtesy of Yale School of Medicine, Emergency Medicine. Femoral Vein

Position the patient as noted previously for examination of the femoral vessels (see Positioning, above). The study begins with an examination of the common femoral vein just distal to the inguinal ligament. The femoral vessels are located just inferior to the inguinal ligament and approximately midway between the pubic symphysis and the anterior superior iliac spine. The femoral artery is usually palpable. This is the initial point of examination.

Apply gel to the transducer, the patient’s leg, or both, and position the transducer transversely, just distal to the inguinal ligament, as shown below. Remember, the indicator on the probe should point toward the patient’s right. In this transverse view, the vein is imaged in cross-section.

Probe positioning for assessment of the femoral vein.

Drag or fan the transducer in a cephalad or caudad direction until the junction of the common femoral vein and the greater saphenous vein can be visualized, as shown below. The common femoral artery is lateral to the common femoral vein.

Ultrasonographic image of femoral vessels without compression.

Using the transducer, apply direct pressure to completely compress the vein. If the vein compresses completely, then a DVT at this site can be ruled out.

Be sure that enough pressure is being applied and being applied evenly. Apply enough pressure so that slight deformation of the artery is noticeable. If the vein is still not completely compressible, a DVT is present. See the image below.

Ultrasonographic image of femoral vessels with compression.

Complete compression of the vein rules out a DVT, whereas the inability to completely compress the vein rules in a DVT. Thus, compressibility is the rule in/rule out criterion for DVT on ultrasound. (See Results, below, for more details.)

Compressibility must be present in both the femoral veins and the popliteal vein. Sometimes, the angle of the transducer may need to be adjusted in order to completely compress the vein. The greater saphenous vein is a superficial vein. A clot in the greater saphenous vein near its junction with the common femoral vein, however, can easily propagate.

The examination of the common femoral vein should extend from 2 cm proximal to 2 cm distal to the intersection of the common femoral and greater saphenous veins. Distal to the greater saphenous vein, the common femoral vein splits into the deep and superficial femoral veins.

Despite its name, the superficial femoral vein is indeed a deep vein. Once collapse of both the deep and superficial femoral veins is confirmed, the examination may move on to the popliteal vein.

Popliteal Vein

Position the patient as noted earlier for examination of the popliteal vessels. (See Positioning, above.)

Again, apply gel to the transducer, the patient’s leg, or both, and position the transducer transversely in the popliteal fossa, with the probe marker directed toward the patient’s right, as shown below.

Probe positioning for assessment of the popliteal vein.

Drag or fan the transducer in a cephalad or caudad direction until the superficial popliteal artery and vein are visible, as shown below. The popliteal vein is usually posterior to the popliteal artery. Given the posterior approach of the probe (transducer face is placed in the popliteal fossa), however, the vein appears more superficial (closer to the transducer face) than the artery. The popliteal vessels are compressed more easily, so reducing probe pressure may help visualize the veins.

Ultrasonographic image of popliteal vessels with clot.

The examination should include the distal 2 cm of the popliteal vein and the proximal aspects of its trifurcation into the anterior tibial vein, the posterior tibial vein, and the peroneal vein. Anatomic variability is not uncommon, and the popliteal vein is often seen dividing into the anterior and posterior tibial veins, with the peroneal vein then splitting off from the posterior tibial vein.

Doppler Ultrasonography

Although not a formal component of the focused lower extremity compression examination for DVT, Doppler ultrasonography may be useful to help determine anatomic orientation and to further interrogate potentially misleading structures. Information obtained from Doppler ultrasonography alone, however, does not yield definitive evidence regarding clot presence.

Doppler examination assesses the direction, velocity, and pattern of blood flow, with venous and arterial vessels demonstrating characteristic patterns. Normal venous vasculature should show venous flow at baseline, augmentation of flow with calf compression, and phasic respiratory ventilation with increased flow during expiration. In general, augmentation helps to assess for obstruction distal to the probe, whereas respiratory variation helps to assess for obstruction proximal to the probe (ie, iliac veins and inferior vena cava).

Some points to keep in mind include the following:

Vessel filling defects may indicate on-site or upstream flow obstructionCysts or other fluid cavities are devoid of flowLymph nodes demonstrate dense, high vascularityPreviousNext, Bedside Ultrasonography in Deep Vein Thrombosis

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