VENOUS ANATOMY

The relevant venous anatomy of the upper extremities and thoracic inlet includes the deep venous system composed of the internal jugular, brachiocephalic (or innominate), subclavian, axillary, and paired brachial veins. The superficial basilic and cephalic veins are also usually included in the examination (Fig. 118-1).

FIGURE 118-1 Venous anatomy of the upper extremity.

In the neck, the internal jugular vein courses from the jugular foramen at the base of the skull lateral to the carotid arteries within the carotid sheath. The internal jugular vein collects blood from the skull, brain, face, and neck. It joins the subclavian vein posterior to the medial clavicle, where it forms the brachiocephalic or innominate vein. A pair of valves is present in its caudal end near the confluence.

The right brachiocephalic vein is approximately 2.5 cm in length and courses in a caudal direction. The left brachiocephalic vein is approximately 6 cm in length, has a more horizontal course, and joins the right brachiocephalic vein to form the superior vena cava.

In the upper arm, the usually paired brachial veins flank the brachial artery. They may join with the basilic vein before forming the axillary vein. The axillary vein begins at the inferior border of the teres major muscle and continues through the axilla to the lateral border of the first rib, where it becomes the subclavian vein. The subclavian vein continues medially, deep to the clavicle, until it joins the internal jugular vein, forming the brachiocephalic vein. Valves may be seen in the subclavian vein near this confluence.

The axillary vein lies medial and inferior to the axillary artery. The subclavian vein is anterior and inferior to the subclavian artery (Fig. 118-2). Knowing these relationships will aid in identification of these vessels and help in distinguishing possible large collaterals from the native vessels.

FIGURE 118-2 Transverse gray-scale (A) and color Doppler (B) images demonstrating the normal anatomic relationship of the subclavian vein (V) anterior and inferior (INF) to the subclavian artery (A). SUP, superior.

PREVALENCE, ETIOLOGY, AND RISK FACTORS

Upper extremity deep venous thrombosis can be divided into primary and secondary thrombosis based on pathogenesis. Primary upper extremity DVT includes Paget-Schroetter Syndrome (effort thrombosis) and idiopathic upper extremity DVT. Secondary upper extremity DVT is found in patients with known inciting causes such as central venous catheters, pacemakers, and malignancy.

The exact prevalence of symptomatic upper extremity DVT in the general population is unknown but is estimated to be approximately 0.2%.² In patients with deep venous thrombosis, approximately 90% involve the lower extremity and the remaining 10% involve the upper extremity.³

With the increasing use of central venous catheters, the prevalence of upper extremity DVT has increased (Fig. 118-3). Earlier studies documented thrombosis in 2% to 12% of patients with central venous catheters.⁴ In more recent studies, upper extremity DVT has been documented in 50% to 60% of patients with central venous catheters. The most powerful independent predictor of upper extremity DVT was the presence of a catheter, with the risk factor increasing sevenfold in these patients.^5,6 The position of the catheter tip has been found to correlate with the incidence of upper extremity DVT. Catheters at the junction of the right atrium and the superior vena cava and those in the mid superior vena cava (SVC) have the lowest incidence of associated thrombosis and those with the catheter tip in the brachiocephalic vein have a higher incidence.⁴ The ideal position for the catheter tip is at the cavoatrial junction. Catheter material and diameter have also been found to affect the incidence of thrombus. The lowest rates have been for polyurethane and silicone catheters and for those with an external diameter less than 2.8 mm.^7,8 In the pediatric population, two thirds of DVT cases occur in the upper extremity, in contrast to adults, and are usually secondary to catheter placement.⁶

FIGURE 118-3 Transverse (A) and longitudinal (B) images show thrombus (arrowhead ) around central venous line (arrow ) in the internal jugular (IJ) vein. C, Longitudinal image shows echogenic thrombus (arrowhead) around peripherally inserted central catheter line (arrow) in the basilic vein (VN).

Cancer is a significant risk factor for upper extremity DVT secondary to alterations in coagulability factors, low-grade disseminated intravascular coagulation, and stasis secondary to tumor compression.⁹ Bilateral upper extremity DVT was found to be more common in patients with malignancy. The risk of thrombosis increases significantly in patients with both cancer and central venous catheters.¹¹

Hypercoagulability (e.g., antithrombin, protein C, and protein S deficiencies; presence of antiphospholipid antibodies) is found to be prevalent in idiopathic upper extremity DVT in which no obvious associated disease or triggering factor is present. In patients with idiopathic upper extremity DVT, 42% to 56% of patients have been found to have clotting abnormalities in recent studies.^6,13,14 Transient causes of hypercoagulability such as estrogen use, pregnancy, and ovarian hyperstimulation have also been observed in women with idiopathic upper extremity DVT.^11,12

Additional predisposing factors for upper extremity DVT include venous stasis, trauma, surgery, sepsis, and thoracic outlet obstruction secondary to anatomic anomalies. Interestingly, conventional risk factors associated with lower extremity DVT, including obesity, advanced age, and surgery were not significant risk factors for patients with non–catheter-related upper extremity DVT.³ Patients with upper extremity DVT were found to be more often male, younger, leaner, and more likely to smoke than those with lower extremity DVT. Recent immobility and prior venous thromboembolism also play less of role in patients with upper extremity DVT; however, cancer was more common.¹³

COMPLICATIONS

The most serious complication of upper extremity deep venous thrombosis is pulmonary embolism (PE). Once thought to be uncommon, PE is now reported to have a prevalence of 7% to 36% in patients with upper extremity DVT.^2,13,14 Clinically, the prevalence of symptomatic PE at presentation has been reported to be fourfold less common in patients with upper extremity DVT when compared with patients with lower extremity DVT. However, after 3-month follow-up, the incidence of major or fatal bleeding, recurrent DVT, recurrent PE, or fatal PE was the same. Not surprisingly, patients with cancer were found to have the worst prognosis. Mortality from PE ranged from 11% to 34%.¹³

Other less common complications of upper extremity DVT include post-thrombotic venous insufficiency, loss of vascular access, superior vena cava syndrome, septic thrombophlebitis and, rarely, venous gangrene.

CLINICAL PRESENTATION

Clinically, the most common presentation of upper extremity DVT is upper extremity and face swelling and pain. The edema is typically nonpitting. Less common signs and symptoms include skin discoloration, a sense of coldness in the hand and forearm, tenderness over the affected vein, paresthesia, and numbness. Malfunction of a central venous catheter may also be an indication of thrombosis. Collateral veins can develop over the shoulder and chest wall. A tender cord may be palpable, especially in the axillary region. These signs and symptoms, however, are nonspecific and confirmation of the diagnosis by objective testing is necessary.¹⁴ In addition, many cases of upper extremity DVT are asymptomatic, especially when related to catheter placement.⁴

IMAGING TECHNIQUE

Traditional x-ray venography, once considered the gold standard for imaging of upper extremity DVT, is a highly accurate examination. However, it is an invasive procedure that must be performed in the radiology department. It is uncomfortable for the patient and venous catheterization may be technically difficult secondary to arm swelling. Moreover, intravenous iodinated contrast administration carries the risk of nephrotoxicity and allergic reaction, in addition to predisposing to the development of thrombus. Venography may also fail to demonstrate the status of the internal jugular or brachiocephalic veins when more peripheral occlusive thrombus is present.

Color Doppler duplex ultrasonography with compression technique has become the imaging modality of choice for the diagnosis of upper extremity DVT and is highly accurate for making this diagnosis.¹⁵ Sonography has the advantage of being noninvasive, requiring no venipuncture, ionizing radiation, or contrast agent. It is a potentially portable examination and can be performed at the bedside for critically ill patients. It can be performed regardless of renal function and serial follow-up examinations are easily done. Unlike venography, the internal jugular and peripheral brachiocephalic veins can be evaluated, despite the presence of thrombus in the more peripheral vessels. Limitations of duplex sonography include inability to visualize the superior vena cava and more central portions of the brachiocephalic veins. In addition, small nonocclusive thrombus may be missed in the subclavian vein secondary to the inability to compress this vessel because of the overlying clavicle.¹⁶ Furthermore, differentiation of a large collateral from the native vein may be difficult in patients with chronic deep venous thrombosis.

The reported sensitivity of color Doppler sonography for the diagnosis of upper extremity DVT has ranged from 78% to 100%, with a specificity of 82% to 100%.^17,18 False-positive examination results are thought to be rare. False-negative results can occur secondary to limitations in the ability to compress vessels (see earlier).

Variations exist in the recommended techniques and protocols for an ultrasound examination of the upper extremity venous system. At our institution, the internal jugular, subclavian, axillary, and brachial veins are imaged, in addition to the superficial basilic and cephalic veins to the level of the antecubital fossa.

The patient is placed supine, with the arm extended but not hyperabducted. The neck is turned slightly away from the side to be examined. Linear 12-5 or 7-4 MHz transducers are used. A curved 5-2 MHz transducer may be required for larger patients to obtain greater depth of penetration and obtain a larger field of view. A compression technique is used, starting with the internal jugular vein. Compression is always performed in the transverse plane because compression in the longitudinal plane may result in sliding off the vessel, potentially causing a false-negative result. All vessels are compressed except where limited by the clavicle.

The vessels are visualized with gray-scale and color Doppler imaging. The internal jugular vein is imaged in the sagittal and transverse planes. The subclavian vein is followed in its entirety and can be imaged from a supraclavicular approach medially and an infraclavicular approach laterally. It should be remembered that the subclavian vein lies anterior and caudal to the subclavian artery. The subclavian vein and artery should be visualized in the transverse plane to ensure the vein’s correct location and proximity to the artery, allowing its differentiation from a large collateral, which will not run adjacent to the artery and will likely have a more tortuous course. The axillary and brachial veins are imaged in a similar manner. The axillary vein lies inferior and medial to the axillary artery. The brachial veins are usually paired and run adjacent to the brachial artery. The basilic vein is single, taking a more superficial and medial course in the upper arm. The cephalic vein courses more laterally. The basilic and cephalic veins run in the subcutaneous tissue, above the muscles of the arm, and do not course adjacent to an artery.

The medial subclavian vein and other centrally situated veins, including the brachiocephalic veins, can be difficult if not impossible to visualize. Use of a square phased-array transducer and a suprasternal-supraclavicular approach may aid in imaging these regions.

Spectral Doppler waveforms are obtained initially in the contralateral internal jugular and medial subclavian veins. These waveforms serve as an internal reference to evaluate for asymmetry, which may be indicative of more centrally located thrombosis not directly visualized by ultrasound examination. Waveforms are then obtained in the ipsilateral internal jugular vein and in the medial, mid, and distal portions of the subclavian vein. If possible, waveforms can also be obtained from the brachiocephalic veins.

ULTRASOUND FINDINGS

Ultrasound imaging of normal venous structures demonstrates complete apposition of the vessel walls with compression (Fig. 118-4). The vessel walls are thin and the lumens are generally anechoic, unless slow flow is present. Normal venous valves are easily visualized as thin leaf-like mobile structures and should not be mistaken for wall-adherent thrombus or sequelae from prior thrombosis.

FIGURE 118-4 Transverse gray-scale split screen ultrasound images show complete compressibility of the normal (A) internal jugular vein and (B) paired brachial veins. BA, brachial artery; BV, brachial vein; CCA, common carotid artery; IJV, internal jugular vein; VC, vein compressed.

Diagnostic criteria for upper extremity venous thrombosis by ultrasound are similar to those described for lower extremity deep venous thrombosis.¹⁹ The principal criterion for the diagnosis of thrombus is noncompressibility of the vessel lumen. Acute thrombus usually fills and distends the involved vessel and is typically anechoic to hypoechoic (Fig. 118-5). Color Doppler flow imaging makes visualization of anechoic and nonocclusive thrombus easier because it permits direct visualization of blood flow dynamics.²⁰ Spectral and color Doppler flow imaging demonstrate absence of flow in the presence of occlusive thrombus (Fig. 118-6). Nonocclusive thrombus will generally be outlined by color and demonstrate some evidence of flow in the vessel (Fig. 118-7).

FIGURE 118-5 A, Split-screen transverse image shows thrombus filling the internal jugular vein (IJV; arrow) which is noncompressible (arrowhead). B, Sagittal image demonstrates the same thrombus (arrows) filling and distending the vessel.

FIGURE 118-6 Longitudinal duplex Doppler image of the axillary vein (arrow) shows absence of flow on color Doppler flow imaging and spectral analysis.

FIGURE 118-7 A, Longitudinal gray-scale image shows nonocclusive thrombus in the internal jugular vein (IJV; arrow). Longitudinal and transverse color Doppler flow images (B, C) demonstrate thrombus outlined by color (arrows). Longitudinal gray-scale (D) and color (E) images of the IJV demonstrate nonocclusive thrombus (arrows), with flow visualized around the thrombus on color Doppler flow images.

The appearance and echogenicity of thrombus will evolve over time (Fig. 118-8). Generally, as thrombus becomes more chronic, its echogenicity increases and the clot retracts, with resultant decrease in the distention of the vessel. The visualized thrombus may be more eccentric and focal in location within the vessel lumen, with skip areas present. The wall may thicken and be incompletely compressible (Fig. 118-9). Although some veins may regain a normal appearance and compressibility over time, other vessels may demonstrate sequelae of chronic venous disease, such as frozen valve leaflets, synechia, and partial recanalization of the vessel. The affected native vessel may collapse and fibrose, with resulting collateral formation. In vessels in which thrombus has resolved, venous insufficiency or reflux may later be present.

FIGURE 118-8 Transverse (A) and longitudinal (B) images of the internal jugular vein in 47-year-old man with neck pain and edema demonstrate occlusive thrombus (arrows). No flow is demonstrated on color Doppler flow imaging (CDFI). C, Follow-up imaging 3 weeks later demonstrates retraction of the clot (arrow), with partial recanalization of the IJV on CDFI. D, E, Follow-up imaging 4 months later demonstrates only a small amount of focal, eccentric, residual thrombus (arrowhead). Note that the IJV has decreased in size. CCA, common carotid artery.

FIGURE 118-9 Transverse color Doppler flow image of the right internal jugular vein shows wall thickening and eccentric thrombus (arrows) consistent with chronic thrombus.

The diagnosis of recurrent thrombosis or acute thrombosis superimposed on chronic thrombosis is problematic by ultrasound. Demonstration of new areas of thrombus not identified on the initial examination and/or considerable enlargement (>2 mm) of the compressed vein diameter between the two examinations have been used as criteria in clinical studies for recurrent lower extremity DVT.²¹ Traditional x-ray or contrast-enhanced MR venography may be necessary for patients with clinically suspected recurrent DVT.

The normal spectral Doppler waveform of the upper extremity and neck veins are characterized by two phasic variations. Right atrial contraction results in a sawtooth pattern to the waveform, which is synchronized to the pulse rate. Superimposed on this cardiac pulsatility is a phasic change in amplitude caused by the respiratory cycle.²² An increase in amplitude and venous return is seen during inspiration and a decrease is noted during expiration (Fig. 118-10). Luminal diameter will also vary with respiration. Sniffing can cause momentary collapse of a normal vessel; a Valsalva maneuver will cause the vessel to distend and velocity of venous flow to decrease.¹⁵

FIGURE 118-10 Color Doppler flow imaging and spectral Doppler imaging show normal cardiac and respiratory variability in the internal jugular (A) and subclavian (B, C) veins.

Although direct visualization of thrombus in the brachiocephalic veins and superior vena cava is difficult, if not impossible, it has been shown that loss or dampening of respiratory and cardiac phasicity in the subclavian and internal jugular veins is a very sensitive predictor of more centrally located thrombus in the brachiocephalic veins or SVC (Fig. 118-11). Loss of cardiac pulsatility has been reported as a more sensitive predictor than loss of respiratory phasicity alone. Conversely, the demonstration of normal cardiac and respiratory phasicity is highly predictive of the absence of thrombus in these vessels.²² Comparison should be made to the waveform in the contralateral subclavian and internal jugular veins to confirm that the abnormal waveform is only present on the affected symptomatic side. Bilateral dampening, however, can occur with thrombosis of the superior vena cava.

FIGURE 118-11 Duplex Doppler imaging in a 66-year-old man with central thrombus in the left brachiocephalic vein. A dampened waveform without respiratory or cardiac phasicity is seen in the mid left subclavian (A) and axillary (B) veins.

PITFALLS

There are limitations in duplex ultrasound imaging of the upper extremity and thoracic inlet venous structures. As noted, considerable constraint is placed by the normal anatomy of the region, with the clavicle, manubrium, and sternum limiting visualization and compressibility of the veins, especially centrally. Compression may also be limited by body habitus, overlying bandages, or indwelling catheters. Nonocclusive thrombus in regions that cannot be compressed may be missed. Color Doppler imaging may aid in the detection of nonocclusive thrombus, but care must be taken not to oversaturate the images with color, which can obscure thrombus (Fig. 118-12).

FIGURE 118-12 A, Longitudinal gray-scale imaging of the right subclavian vein shows nonocclusive thrombus (arrow). B, Oversaturation on color Doppler flow imaging obscures the thrombus.

Slow-flowing blood can appear echogenic and mimic thrombus (Fig. 118-13). One should look carefully for swirling or slow-moving particles on real-time imaging, the presence of which will distinguish slow-flowing blood from true thrombus. Compressibility of the vessel will also confirm absence of thrombus.

FIGURE 118-13 Echogenic material is seen on longitudinal (A) and transverse (B) images of the right internal jugular vein (IJV), which mimics thrombus (arrows). The echogenic material was seen to swirl on real-time imaging. B, Axial imaging demonstrates the vessel compressing completely (arrowhead). C, Longitudinal color Doppler imaging shows no evidence of flow void in the IJV. CCA, common carotid artery.

Large collaterals can be mistaken for the native vessels, especially in the subclavian region. Proximity to the accompanying artery and the correct anatomic relationship between artery and vein should be looked for in the transverse plane.

SYNDROMES

Thoracic Outlet Syndrome

Thoracic outlet syndrome (TOS) can be defined as a set of symptoms caused by compression of the brachial plexus structures or vascular structures (subclavian artery and vein) as they pass from the lower cervical region or thoracic outlet to the axilla. It is more common in women than in men and occurs most commonly in the 20- to 50-year-old age range. An understanding of the anatomy of this region is helpful in understanding the pathophysiology of this syndrome.

The anatomy of the thoracic outlet region can functionally be thought of as composed of three areas of narrowing: (1) the interscalene triangle; (2) the costoclavicular space; and (3) the subcoracoid or retropectoralis minor space (Fig. 118-14). The interscalene triangle is bounded by the anterior and middle scalene muscles and the first rib to which they are attached. The three trunks of the brachial plexus and subclavian artery pass through this region. The subclavian vein passes anterior to the anterior scalene muscle. The divisions of the brachial plexus and subclavian artery and vein then travel under the clavicle into the costoclavicular space, which lies between the clavicle and underlying first rib and is bounded anteriorly by the subclavius muscle. These structures enter the axilla through the subcoracoid (retropectoralis minor) space, bounded by the coracoid process and insertion of the pectoralis minor muscle superiorly and anteriorly and by the ribs posteriorly.

FIGURE 118-14 Anatomy of the thoracic outlet. A, interscalene triangle; B, costoclavicular space; C, subcoracoid (retropectoralis minor) space.

Compression and irritation of neural and vascular structures by repetitive movement and/or arm elevation can occur in these regions of narrowing. The interscalene triangle is the most common site of entrapment. The subclavian vein and artery are most often compressed at the costoclavicular space.²³ Anatomic variants such as cervical ribs, hypertrophy of the C7 transverse processes, and cervical bands can also result in entrapment.²⁴

Clinically, the symptoms of thoracic outlet syndrome can be neurologic or vascular. Neurologic symptoms include pain (especially in an ulnar distribution), paresthesia, numbness, loss of dexterity, weakness, and occipital headache. Venous symptoms include upper extremity swelling and cyanosis. Claudication, pallor, and coldness can result from arterial compromise.

Provocative tests such as Adson’s maneuver—checking the radial pulse with the shoulders depressed downward, head hyperextended and turned toward the affected side—and arm hyperabduction may aid in the diagnosis but demonstrate overlap in positive findings (variation in strength of the radial pulse during positional changes) with asymptomatic individuals.

Color Doppler sonography has been found to be a useful aid for the diagnosis of TOS because it allows direct visualization of the vessels in conjunction with spectral Doppler waveforms during maneuvers designed to result in vascular compression.²⁴ Longley and colleagues²³ have found that in symptomatic patients with thrombosis or significant compression of the subclavian vein during arm abduction (90 to180 degrees), color Doppler sonography has a sensitivity of 92% and a specificity of 95% for the detection of thoracic outlet syndrome. Criteria used in this study for a positive result were detection of thrombus or change in the Doppler waveform, from a normal subclavian waveform to one showing complete loss of cardiac and respiratory pulsatility or cessation of flow. Evaluation of the subclavian artery yielded less helpful results, with 20% of asymptomatic individuals demonstrating changes in Doppler waveform on hyperabduction.

Venous imaging using CT angiography (CTA) or MR angiography (MRA) of TOS may also be useful, with imaging performed with the patient’s arms alongside the body and then elevated over the head. Comparison of vascular patency using multiplanar and three-dimensional reformations of CTA or MRA can provide evidence for TOS. With CT or MRI, evidence of bony or soft tissue impingement on the brachial plexus can also be assessed. This technique has been found to be useful in evaluating the arterial structures but is less helpful in evaluating venous compression secondary to overlap of findings with asymptomatic individuals.²⁵

Ultrasound offers the advantage of allowing visualization of the vessels during dynamically induced symptoms. Ultrasound also allows for imaging the patient in an upright or seated position, similar to a clinical examination, as opposed to CT or MRI, which have to be performed with the patient supine. Disadvantages include limited evaluation of the surrounding soft tissue and bony structures, especially in the region of the pulmonary apex.²⁵

Lemierre’s Syndrome

Lemierre’s syndrome is a septic thrombophlebitis of the internal jugular vein usually caused by the anaerobic gram-negative rod Fusobacterium necrophorum, although other strains of fusobacterium have been implicated.²⁸ F. necrophorum makes up part of the normal flora of the mouth. Lemierre’s syndrome is an uncommon sequela of acute pharyngotonsillitis that can be potentially life-threatening. Infection from the oropharynx may spread by direct extension to the parapharyngeal space or through venous or lymphatic dissemination. Thrombophlebitis of the internal jugular vein results from the surrounding inflammation and acts as a nidus for further septic embolization and septicemia. The lungs and joints are common locations for septic emboli and abscesses.²⁸ The first series of cases was described by Lemierre in 1936. In the preantibiotic era, the mortality rate for the condition was 90%.²⁹

Generally more common in young healthy adults, clinical signs and symptoms can be nonspecific. Patients typically present with pharyngitis but this may be absent in some cases. Fever, rigors, cervical adenopathy, and malaise are common accompanying symptoms. Because of their proximity to the carotid sheath, cranial nerves IX to XII may be affected, with associated neurologic signs and symptoms. In later stages, symptomatology is related to the location of the septic emboli.^28,30

Ultrasound or CT imaging demonstrates thrombus within the internal jugular vein (Fig. 118-15). Surrounding inflammatory changes in the parapharyngeal region are best demonstrated by CT, as are septic emboli in the chest.

FIGURE 118-15 Transverse contrast-enhanced CT image through the mid neck demonstrates edema and inflammation (*) involving the left parapharyngeal region. The left internal jugular vein (arrowhead) is occluded. The arrow indicates the common carotid artery. LN, enlarged lymph nodes.

CONCLUSION

Although initially thought to be an uncommon, benign, and self-limited entity, upper extremity deep venous thrombosis is now known to be a fairly frequent condition, with significant resulting morbidity and mortality. The increased use of central venous lines and catheters, especially in patients with associated malignancies, has resulted in a dramatic increase in the occurrence of upper extremity DVT. Color Doppler sonography has proven to be a highly accurate imaging modality for screening, diagnosis, and follow-up of this entity, effectively replacing the traditional gold standard of invasive venography. Spectral and color Doppler sonography have also been found to be of benefit in the diagnosis of thoracic outlet syndrome. They can complement MRI and CT imaging, especially in the diagnosis of possible venous involvement.

KEY POINTS

Upper extremity deep venous thrombosis (DVT) has a much higher prevalence than originally thought, especially in the patient population with central venous catheters, underlying malignancy, and hypercoagulability states.

Pulmonary embolism is the most serious complication of upper extremity DVT and has been reported in up to 35% of patients with upper extremity DVT.

Color Doppler duplex sonography with compression technique is the imaging modality of choice for the diagnosis of upper extremity DVT.

Loss of phasicity in the spectral Doppler waveforms in the internal jugular or subclavian veins can be indicative of more central thrombosis.

Color and spectral Doppler imaging, along with CT and MRI, can aid in the diagnosis of thoracic outlet syndrome.

Patients with Paget-Schroetter syndrome need to be treated more aggressively with thrombolytic therapy because the risk for developing long-term sequelae, such as post-thrombotic syndrome, is higher.