Fundamentals

A systemic CVO is a complete blockage of in-line flow in a large systemic venous conduit of the central body cavities (chest, abdomen or pelvis). The transition to a central venous branch in the upper and lower body occurs at the thoracic outlet in the chest and inguinal ligament in the abdomen and pelvis. The superior and inferior vena cava (SVC and IVC) are the most central and sizeable veins of the systemic circulation above and below the diaphragm. These sustain venous return into the right atrium (RA) alongside the pulmonary circulation to the left atrium. The cavae and adjacent major central systemic veins make up the outflow for visceral, superficial and deep systemic branches of the head and neck (H&N), peripheral extremities, and trunk. Branches from the upper body ultimately converge into the Superior Innominocaval (SIC) system in the thorax and from the lower body into the Inferior Iliocaval (IIC) system in the abdomen and pelvis ( Table 1 ). The portal system is a unique somewhat autonomous collection of visceral drainage, including the gastrointestinal, pancreaticobiliary and splenic veins which conventionally flow into the liver prior to emptying into the IIC via the hepatic veins. CVOs in each distribution have specific etiologies and regional manifestations that dictate the presentation, diagnosis, and management. Notable examples are SVC syndrome (SIC), lower extremity venous insufficiency (IIC) and Budd-Chiari with portal hypertension (hepatoportal system and IIC). An especially concerning scenario that affects both distributions is FFT and CIT in the RA. These pose substantial morbidity and mortality with the most feared sequela being a massive pulmonary embolus. In select patients endovascular intervention using large bore aspiration catheters under IVUS guidance has been shown to be safe and effective for RA thrombectomy. This paper will review the use of IVUS in CVR for occlusions in the SIC and IIC distributions and briefly touch upon the portal system and RA thrombectomy. Before covering the technical aspects of IVUS, it is necessary to review relevant pathophysiology and anatomy.

Pathophysiology

Venous occlusions manifest from three basic mechanical processes :

• 1.
  

  Intraluminal obstruction from thrombus, hyperplasia, devices, or tumors.

  
  
• 2.
  

  Extraluminal compression from a viscera, vessel, mass, collection, hardware, or musculoskeletal tissue causing intermittent or fixed venous effacement.

  
  
• 3.
  

  Stricture formation from intrinsic vein wall injury resulting in reactive fibrotic wall thickening, contracture, and eventual obliteration of the lumen.

The underlying pathologies that drive an occlusion are broadly divided into benign or malignant etiologies, which portend different treatment approaches and prognosis. The most frequent benign pathologies are hemodialysis related complications, provoked and unprovoked deep venous thrombosis (DVT), device related thrombophlebitis with fibrosis (catheters, IVC filters, and cardiac leads), and compression syndromes (Thoracic outlet, Nutcracker, and May-Thurner). Common malignant CVOs come from invasion and/or compression by lung cancer (NSCLC), lymphoma, thymic cancer, liver tumors (HCC), renal cancers (RCC), adrenal carcinoma, germ cell tumors, leiomyosarcoma and gynecologic tumors. Chronic CVOs often involve all three elements since etiologies that cause intraluminal obstruction and compression lead to strictures and vice versa. For example, a compressive May-Thurner that causes an occlusive stricture in the left common iliac vein with DVT extending peripherally from the occlusion into the ipsilateral extremity veins. It is important to note that DVTs are both a cause and effect of benign and malignant CVOs due to stimulation of Virchow’s triad (stasis, injury and hypercoagulability).

Anatomy

Venous Variations

Inherent anatomic differences and physiological effects are known to influence the normal caliber, flow, and appearance of central systemic veins on imaging. Anatomic differences are static variations between patients with the following factors reported in the imaging literature:

• •
  

  Gender: Male veins are thought to be 1-2 mm larger in average diameter, however conflicting CT based data shows the IIC veins are up to 2 mm larger in females of equivalent size. Also, the gonadal and pelvic veins differ in women and lend to higher rates of pelvic congestion and lower extremity venous insufficiency related to pregnancy.

  
  
• •
  

  Body Habitus and Age: A positive linear correlation is noted with Height and Weight for larger diameter and length, but the correlation with Age is less clear.

  
  
• •
  

  Morphology: Venous flaring at junctions and confluences (ex. cavoatrial junction, supra-azygous SVC and suprarenal IVC) results in nonuniform diameters.

  
  
• •
  

  Laterality: Vein diameter is greater on the Right by approximately 1-2 mm and has potential correlation with limb dominance, but length and angulation are greater on the left given crossover to right-sided cavae and azygous veins (ex. left innominate, renal, hemiazygous, lumbar and iliac veins). Left tributaries also differ, such as the gonadal and adrenophrenic veins which drain to the renal vein on the left and IVC on the right.

  
  
• •
  

  Congenital variants

  
  
  
  
  • ○
    

    Fenestration- Short segment division of a branch with reconvergence before terminal drainage

    
    
  • ○
    

    Duplication- Separate branches with distinct origins and/or terminal drainage (partial or complete)

    
    
  • ○
    

    Situs reversal (ex. Left SVC or IVC with or without congenital heart disease)

    
    
  • ○
    

    Interruption, agenesis, or absences of a segment/branch (ex. azygous continuation of the IVC)

    
    
  • ○
    

    Compression syndromes (ex. Paget-Schroetter, Nutcracker, May-Thurner and Popliteal entrapment)

  
  

Dynamic physiological variations can continuously or transiently influence the appearance and measurement of normal and abnormal veins on imaging as well. This includes:

• •
  

  Volume status- Diameter shows a significant positive linear correlation only when extreme volume shifts are reached (ex. hemorrhagic shock or cardiac/renal overload), but otherwise the majority of volume shifts cause < 1 mm difference (eg, NPO for sedation)

  
  
• •
  

  Cardiac cycle- End systolic > End diastolic diameter by 1-4 mm

  
  
• •
  

  Inflow: Increased with visceral function (ex. postprandial portomesenteric flow and postexercise skeletal vasodilation) and Hemodialysis arteriovenous fistula

  
  
• •
  

  Position

  
  
  
  
  • ○
    

    Abduction and flexion of the shoulder (compress subclavian vein) and hip (compress common femoral vein)

    
    
  • ○
    

    Prone (Multifactorial, but favored to increase venous return)

    
    
  • ○
    

    Trendelenburg (Upper > Lower vein distension) and Reverse Trendelenburg (Lower > Upper vein distension)

    
    
  • ○
    

    Ipsilateral neck rotation (compress internal jugular vein)

  
  
  
  
• •
  

  Respiratory phase: Expiratory venous pressure and diameter > inspiratory

  
  
• •
  

  Pregnancy: Fetal circulation increases venous volume and diameters, and mass effect compresses IIC veins.

Knowing the pathophysiology, anatomy and variations of veins, particularly the normal course and caliber, is essential to using IVUS successfully during CVR. ^{, ,}

Clinical Presentation and Indications

CVOs can present with a wide range of clinical findings. The most common symptoms are from subacute to chronic venous congestion downstream of the occlusion. However, more worrisome findings of organ dysfunction do occur and can be life-threatening, especially when venous return to the heart is significantly diminished. The exact prevalence of CVOs is not well known as they can be incidental imaging findings in asymptomatic patients. ^{, , ,} This is due to highly effective networks of collateral drainage that reflexively dilate to bypass an in-line blockage and maintain venous return to the heart. CVOs that occur gradually allow for progressive maturation of collaterals, providing equal outflow to obviate venous congestion. Even acute or subacute symptoms from a rapidly progressive CVO can be mitigated by collateral formation overtime, especially with effective anticoagulation to reduce superimposed thrombosis and progression of disease. However, there are many patients in which collateralization and conservative measures are inadequate. This is more common with extensive and progressive CVOs that eliminate available bypass points that prevent collaterals from forming. This not only causes inadequate compensation and notable symptomatic congestion but increases the likelihood of thrombosis and organ dysfunction. A common scenario is when an inciting event (injury, illness, surgery, a period of prolonged immobility) triggers Virchow’s triad, causing acute on chronic progression of a CVO with superimposed thrombosis. This results in more urgent and even emergent presentations.

The core symptoms of venous congestion commonly develop in the upper or lower extremities with swelling (nonpitting edema > pitting), heaviness, pressure-like pain, numbness, tingling, warmth, redness and reduce mobility. Prolonged CVO in the SIC and IIC will eventually cause post-thrombotic syndrome and venous insufficiency from valvular dysfunction and reflux. Data shows a 40%-60% likelihood of inducing moderate to severe PTS (edema, claudication, immobility, ulceration and infection) within 2 years. Clinical scoring using the CEAP classification and Villalta system can help in assessing severity and the benefit of intervention. Patients who exhibit C4 disease (stasis dermatitis) or greater and have moderate or higher Villalta scores generally benefit from intervention both inpatient and outpatient, especially those with nonhealing venous ulcers. Emergent inpatient intervention is usually reserved for venous ischemia with acute phlegmasia. On exam patients can begin with less severe findings of cerulae albens (a milk-white extremity with intact sensorimotor exam), but progress to critical cerulae dolens (purple cyanotic extremity with sensorimotor deficits). CVOs portend a higher risk of phlegmasia than peripheral DVT given the reduction in available collateral pathways. Significant venous pressure more easily builds escalating from vague discomfort and swelling to tense edema with neuropathy, cyanosis and ischemic tissue loss within 6-12 hours from symptom onset. Patients with thrombotic CVO are also at risk for pulmonary emboli (PE) more so in the IIC distribution than the SIC veins. Studies estimate up to 12% of caval thromboses having concomitant PE diagnosed at presentation or on subsequent imaging. Debate exists regarding the comparative risk of PE in the setting of high-risk free-floating clot or clot in-transit, but the literature favors the risk of PE is increased.

Thoracic CVOs of the SIC distribution result in the unique constellation of SVC syndrome, including swelling with facial plethora and visible venous distension in the H&N (increased jugular venous pressure), cough (dry), hoarseness, dysphagia, orthopnea, dyspnea, conjunctival suffusion, vision changes, papilledema, headache, tinnitus, cyanosis, presyncope (lightheadedness and dizziness), syncope, hypotension, altered mental status, stupor and coma. SVC syndrome can be graded from 0-4 (asymptomatic to life-threatening coma and hypotension) using the classification by Yu et al. in 2008 with the most common findings being facial edema. Life-threatening symptoms develop more so when in-line SVC and collateral AzV drainage are both occluded, which critically impairs venous return to the right heart. Inadequate preload and pulmonary perfusion lends to hypotension and hypoxemia while severe congestion causes coma and respiratory distress from cerebral and laryngeal edema. This creates a vicious cycle where intubation and volume resuscitation, though necessary, could cause cardiovascular collapse and brain death. Malignancy accounts for 60%-70% of SVC occlusions, particularly lung cancer, with remaining occlusions being benign device related fibrosis and thrombosis (cardiac leads and central venous catheters). Indwelling cardiac leads regularly form fibrin sheaths and thrombus that promote CVO in the SIC. Patients who develop significant congestion in the ipsilateral extremity can undergo CVR with IVUS. However, interventions are usually limited to venoplasty without stenting. Treatments beyond this require a multidisciplinary approach involving the electrophysiologist and cardiothoracic surgeons for potential laser-assisted lead extraction followed by endovascular reconstruction. Hemodialysis patients are another unique subset that frequently suffer from benign CVO in the SIC veins due to long dwell times of dialysis catheters, continuous high flow from fistulas and grafts and thrombotic complications of accesses. When a CVO is in-line with a dialysis access the symptoms of venous congestion are magnified by the high flow. Moreover, long standing CVOs result in access malfunction with difficult cannulation due to swelling and pain, prolonged bleeding, aneurysmal degeneration, high pressures and recirculation. Prior to any CVR it is critical to know if a patent fistula or graft is present given the much higher risk of morbidity and mortality with rupture or bleeding in an arterialized venous system.

Abdominopelvic CVOs of the IIC distribution also have special features outside of the lower extremities. Swelling and superficial venous dilation can develop circumferentially in the abdominal wall and lower back, especially with IVC involvement. Impaired drainage and occlusion of the gonadal, renal or hepatic veins can cause concomitant pelvic congestion syndrome, renal failure with hematuria and oliguria and Budd-Chiari with liver dysfunction. Pericaval abdominal malignancies, notably renal cell carcinoma (RCC), are a common etiology alongside prolonged IVC filtration and central venous access. Less common etiologies include trauma, surgery, infection, vasculitis, hypercoagulable disorders, pregnancy, renal disease, drugs and dehydration. CVO of the IIC can propagate clot antegrade and retrograde with clot begetting clot exponentially as venous outflow and inflow is progressively reduced. Due to the capacitance of the iliocaval system, a significant burden of thrombus can build asymptomatically until a critical flow-limitation is reached, causing a symptomatic acute on chronic occlusion. At the time of symptomatic detection, a mix of acute (<14 days), subacute (14-28 days) and chronic (> 28 days) thrombus is present in radial layers with softer acute to subacute clot at the central laminar flow and chronic fibrinous clot adhering to the vein wall. Enhancing tumor thrombus should also be suspected when invasive and thrombogenic pericaval cancers, especially RCC, capable of thrombosing the high capacitance iliocaval system are seen on imaging. It is important to be aware of these associations and their pathophysiology to appropriately diagnose and treat CVO of the IIC.

Occlusions of the portal system (PVO) are a unique subset of CVO in the abdomen and pelvis that can involve the mesenteric and splenic veins. Benign etiologies, including cirrhosis, hypercoagulability, pancreatitis, GI infection and inflammation, are more common than malignant occlusions, such as hepatocellular and pancreatic cancer. PVOs can present with abdominal pain, ascites and varices along portosystemic collateral pathways that can bleed. Subacute to chronic mesenteric ischemia can develop causing postprandial pain, anorexia, bleeding, nausea, vomiting and weight loss. However, rarely acute bowel ischemia and infarction do occur and should be suspected in patients with an acute abdomen, sepsis and lactic acidosis. PVO are extremely problematic in cirrhotic patients and often require portal vein recanalization and even creation of a transjugular portosystemic shunt (TIPS) prior to transplantation.

Catheter malfunction and associated thrombosis is an increasingly common presentation warranting CVR in both the SIC and IIC distributions. CVR with IVUS can be used to restore function or open central veins to facilitate placement of a catheter. Occlusions from fibrin sheaths, thrombus and strictures impair aspiration and flushing and cause symptomatic venous congestion. The likelihood of CVO increases with larger French catheters, longer dwell times, greater traversed venous length (PICCs), smaller access vessel, placement across a compression point (TOS) and malposition, especially retracted dialysis catheters that subject the SVC to high flows. ^{, , , ,}

Preoperative Imaging

Once clinical concern is present, diagnosis of CVO begins with noninvasive imaging, including a duplex ultrasound of the upper or lower extremity veins (US) and a computed tomographic venogram (CTV). US is often the first test ordered given peripheral DVT symptoms are the most recognizable. Veins can contain acute hypoechoic central clot with venous expansion or chronic echogenic eccentric clot with venous contraction. Specific findings of occlusive (noncompressible) DVT extending centrally into the SIC or IIC veins with loss of respiratory phasicity should trigger a CTV to evaluate the central veins. Adequate contrast filling of the veins on CT requires a minimum of a 2–3-minute delay to distinguish pathology from artifactual mixing of unenhanced venous blood. On CTV acute to subacute clot maintains or expands the venous caliber but generally lacks mature superficial and deep collateral drainage pathways. Conversely, venous stenosis, calcification and large collaterals favor a more chronic occlusion (>28 days), particularly when an obstructing tumor or intravascular device is present. Unfortunately, clot density by Hounsfield units can be variable, but use of dual-energy and spectral CT is being studied for this purpose. However, often mixed chronicity thrombus is present at the time of detection. A CT angiogram of the pulmonary arteries (CTA-PA) and echocardiography should be considered for both emboli and clot in transit, particularly in patients with intracardiac extension of thrombus and hemodynamic sequela of PE or heart failure. Identification of the underlying etiology is critical as well, especially in the setting of malignancy. Contrast enhanced Magnetic Resonance Imaging (MRI) can help differentiate tumor invasion and thrombus from benign CVO. MRI also has a role for reducing radiation dose, particularly in young females, and obtaining noncontrast time of flight imaging in those with contrast allergies and renal dysfunction. Its use, however, is limited by long acquisition times that are hard for patients with symptomatic CVOs to tolerate. ^{, , , , , ,}

Additional Preprocedure Evaluation

In addition to the relevant past medical history, review of symptoms and physical examination as detailed above, it is important to confirm if a patient is allergic to contrast, latex, lidocaine, sedatives, heparin/anticoagulants and metals contained in stents and devices (namely Nickel) and adjust accordingly.

Early initiation of anticoagulation using heparin or low-molecular weight heparin and continuation during the procedure is paramount to reducing disease progression and complications from thromboemboli. Active bleeding and other contraindications to anticoagulation and thrombolytics (recent intracranial hemorrhage, surgery, trauma, aortic pathology, coagulopathy and severe thrombocytopenia) must be reviewed as well prior to CVR and could require expert consultation (usually hematology or vascular medicine).

Active infection must also be ruled out, particularly septic thrombophlebitis and cellulitis in affected extremities. Appropriate antibiotics should be initiated prior to intervention and ideally blood cultures should be clear. Of course, scenarios exist where CVR using IVUS is necessary to extract thrombus or occlusive venous device that is a persistent source of infection. The risks and benefits of such a procedure would necessitate the input of an infectious disease specialists for confirmation of the site and medical optimization. In the case of an infected thrombosed hemodialysis access consultation with vascular surgery is warranted given open surgical thrombectomy and debridement are often necessary.

With regards to sedation, most CVR with IVUS are done under general anesthesia given the inherent length and associated discomfort, but also for support in case of complication, such as pulmonary emboli or SVC rupture causing tamponade and shock. An exception to this is May-Thurner interventions, which can be tolerated under moderate sedation. All patients should have an ASA and Mallampati score performed and be assessed for hemodynamic stability, right heart dysfunction, oxygen demand, OSA and ability to lay flat. In the case of right heart strain and SVC syndrome monitored anesthesia care (MAC) without intubation is the safest route for sedation to avoid cardiovascular collapse. However, experts in cardiac anesthesia can perform intubation safely if deemed necessary. preoperative Labs include a CBC (Hgb >7 and Plts > 30 K), CMP (Cr, GFR and LFTs), Blood cultures, Lactate and Coagulation panel (INR, PT, PTT and/or Xa levels) and a pregnancy test. Interventions requiring exposure to x-ray, contrast and sedation in pregnant patients are generally avoided during the sensitive 1st trimester. However, the use of IVUS can mitigate this exposure to the fetus if intervention is necessary. Acute and chronic renal failure should also be assessed before intervention given the possibility of progression with iodinated contrast. Although contrast exposure can be significantly reduced with the use of IVUS, the risks and benefits must be weighed carefully in patients who are not on dialysis. This could require input from nephrology to determine safety and to aid with counseling the patient.

General Considerations for IVUS

IVUS is a reliable tool to tackle the extensive static and dynamic variations found within normal and pathological veins. As highlighted above, the wide quantitative ranges in the literature preclude extrapolation of sampled venous metrics across patients. Moreover, findings from preprocedural CT and US imaging can evolve by the time an intervention is underway. IVUS allows interventionalists to obtain live cross-sectional ultrasonic images of a CVO to more accurately and precisely treat the individual needs of a patient. Although very helpful for venous mapping, the quality of static or pullback venography at select segments can vary with contrast injection, flow impedance (by sheaths and pathology), variable breathing, cardiac function, motion, radiation exposure and digital calibration. In contrast, IVUS images are only influenced by gain, FOV and infrequent artifacts from adjacent structures (ex. ring down). These are easily overcome using digital adjustments and over the wire centerline positioning. IVUS also provides continuous 360-degree intraluminal imaging across multiple locations and time points. This enables qualitative and quantitative evaluation of a vein’s cross-section throughout the cardiac and respiratory cycle without significantly adding radiation or contrast. ^,

Transverse 2-D cross-sectional measurements provide accurate maximum and minimum values of both the luminal and wall to wall area and caliber. Additionally, direct sonographic visualization better discriminates between pathologies, particularly DVT and fibrotic strictures (both of which appear similarly as absent filling on venography), and evaluates vein wall integrity and perivenous tissues to distinguish malignant compression and invasion from benign compression syndromes. Furthermore, it can identify points of rupture with hematoma that have undergone tamponade and are not visible by venography, but still at risk for progression with venoplasty. Continuous dynamic assessments with IVUS also allow for simultaneous evaluation during augmentation of venous volume (infusion of saline), inflow (calf or hand squeeze) and positioning (neutral vs provocative maneuvers). With this range of venous distension and flow it is easier to differentiate transient vasospasm, compression and physiological under distension from true fixed CVOs with slow echogenic flow. Moreover, aggregate measurements of CVOs can be obtained at varying levels of distension to establish an accurate steady state caliber to guide balloon and stent sizing.

General Procedure Steps

Initial selection of the venous access points is critical for successful CVR with IVUS. For nearly all CVOs, and especially those involving the cavae, recanalization is safest when done through dual antegrade and retrograde access. The best vessels to access are in-line patent peripheral veins with the shortest and straightest course to the CVO. This usually includes the Internal Jugular, Brachial, Basilic, Cephalic, Common Femoral, Greater saphenous and Popliteal veins with the right side having more favorable angulation. In many instances the access point also factors in the need for additional recanalization to restore inflow from the periphery to maintain central venous patency. Appropriate selection optimizes geometric alignment for more stable crossing systems capable of pushing and steering through the center of a tough CVO. Co-axial or Tri-axial hydrophilic braided crossing systems (9 Fr base sheath, 6 Fr guide sheath, and 4-5 Fr tapered catheter) can be advanced from both directions until the sheath and catheter reach each end of the occlusion. ^, At this point heparinization should be considered with the ACT maintained between 230-250 seconds.

Both blunt and sharp recanalization can then be attempted from above or below with a target in the opposing patent end to guide traversal in the true lumen. Venography and over the wire radial IVUS should be used to identify a concavity or nub at the cranial or caudal margin of the occlusion. If present the sheath can be pointed directly at this point to support seeding the tip of a 4-5 French catheter into the nub. A standard or stiff Glidewire should then be driven a short length into occlusion without dislodging the support system. Fluoroscopically it will appear as if the wire exited the catheter and immediately stuck into a tight space. Resistance with movement of the wire or catheter suggests appropriate seeding within the occlusion. The wire can then be spun using a rotary motion to slowly drill through the occlusion. A similar degree of resistance should remain until the wire reaches the target at the opposing patent end. If the wire stops advancing and begins buckling back, then carefully track the catheter as far along the wire as possible without causing it to retract. To aid in trackability the catheter can be gently spun over the wire to help bore through. A sudden loss of resistance or an atypical wire course prior to reaching the patent end raises concern for extravascular perforation, especially if no collateral is present in the region. A safe and easy way to confirm if the wire has reached the target is by placing IVUS in the opposing true lumen. If it is not seen sonographically and oblique fluoroscopic projections show malalignment, then the wire should be retracted to the point just before the resistance was lost and then redirected back into a point of resistance prior to drilling forward. Several tries using blunt recanalization with an array of wires and crossing systems should be attempted prior to transitioning to a sharp technique. ^{, ,}

Sharp techniques are best suited for short relatively straight native CVO, but longer in-stent occlusions can be safely traversed with a sharp approach. The tools available for sharp recanalization in escalating order are the Back end of a stiff 0.014-0.035” wire, Needle cannulas/sheaths (Colapinto 16 G, Rosch-Uchida 14 G, Chiba, Trans-septal) and PowerWire Pro radiofrequency guidewire. Both radial and side-firing IVUS can be used for targeting and direct visualization of entry in the opposing lumen. Adjacent side-firing catheters have the added ability to monitor a sharp trajectory in real-time. By deflecting the tip, the sector can be positioned to view across the entirety of the recanalization length with all 3 available tools for sharp approaches appearing echogenic. It is also feasible to place an easy to reach target, such as a balloon, snare or Amplatzer plug next to the IVUS catheter.

Once wire is visibly across to the other end on IVUS a snare can be used to establish stable through and through access. The wire can then be exchanged for a rail or working wire, such as 0.035” exchange length 260 cm Ampltaz or 450 cm Dreamwire. IVUS is then advanced across the unopacified occlusion to confirm the true lumen was traversed and evaluate the underlying pathology. Predilation can be done with a 4 mm balloon to improve trackability of the IVUS catheter through the CVO if necessary. Visualization of the catheter within intact vein walls and identification of normal adjacent vessel segments and perivenous structures helps to confirm recanalization through the true lumen ( Fig. 1 ). For example, seeing a pulsatile iliac artery parallel to the target iliac vein supports an in-line intraluminal course.

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