Internal Jugular Vein Thrombosis 

Updated: Mar 27, 2020
Author: Dale K Mueller, MD; Chief Editor: Vincent Lopez Rowe, MD 

Overview

Background

Internal jugular (IJ) vein thrombosis refers to an intraluminal thrombus occurring anywhere from the intracranial IJ vein to the junction of the IJ and the subclavian vein to form the brachiocephalic vein. It is an underdiagnosed condition that may occur as a complication of head and neck infections, surgery, central venous access, local malignancy, polycythemia, hyperhomocysteinemia, neck massage, and intravenous (IV) drug abuse. It is also reported to occur spontaneously.

Currently, with the widespread use of the IJ vein for venous access, central venous catheters are the most common underlying cause of IJ thrombosis. Of concern is a trend reflecting a growing number of IV drug abusers who present with IJ thrombosis secondary to repeated drug injection directly into the IJ vein. Other causes include local malignancies and head, neck, and cardiac surgical procedures. Rare causes include polycythemia, hyperhomocysteinemia, and neck massage.

IJ thrombosis itself can have serious potentially life-threatening complications, including systemic sepsis, chylothorax, papilledema, airway edema, and pulmonary embolism (PE).[1] Secondary infection of the thrombosis may result in septic thrombophlebitis. An infected IJ thrombus caused by extension of an oropharyngeal infection is referred to as Lemierre syndrome; this has also been termed necrobacillosis or postanginal septicemia.

The diagnosis often is highly challenging and requires, first and foremost, a high degree of clinical suspicion. The best approach to making the diagnosis once suspicion is raised has not been definitively established.

The morbidity and mortality of IJ vein thrombosis are comparable to those of upper-extremity deep vein thrombosis (DVT); accordingly, consideration should be given to treating these two entities in a similar fashion.

Thrombolytic treatment has rarely been used to treat IJ vein thrombosis.

For patient education resources, see the Lung Disease and Respiratory Health Center, as well as Pulmonary Embolism, Venous Access Devices, Phlebitis, and Blood Clot in the Legs.

Anatomy

The IJ vein begins in the cranium at the conclusion of the sigmoid sinus. It exits the cranium via the jugular foramen and then courses through the anterior neck lateral to the carotid artery, covered by the sternocleidomastoid muscle for most of its length. It concludes by joining the subclavian vein, thus forming the brachiocephalic vein.

The styloid process divides the lateral pharyngeal space into an anterior (muscular) compartment and a posterior compartment containing the carotid artery within the carotid sheath, the IJ vein, cranial nerves IX-XII, and lymph nodes.

Pathophysiology

The classic triad predisposing to intravascular thrombosis was described first by Virchow and includes the following:

  • Blood vessel trauma
  • Stasis of blood flow
  • Hypercoagulable state

In the case of central venous lines, the catheter itself acts as the nidus for clot formation, despite being bonded and flushed with heparin. Additionally, the catheter tip itself may produce damage to the vessel wall and disrupt venous flow, further augmenting clot formation.

Various oropharyngeal infections (eg, odontogenic infections and infections of the tonsils, peritonsillar tissue, pharynx, sinuses, middle ear, and parotids) may lead to Lemierre syndrome. The primary infection spreads to the posterior compartment of the lateral pharyngeal space, leading to thrombophlebitis of the IJ vein. The infection spreads via local tissue planes, venules, or lymphatic vessels. Subsequent sepsis syndrome may occur, usually a week or more after the primary infection.

The factors responsible for bacterial invasion are not well understood, though bacterial toxins, primary viral infection, and smoking have all been implicated.

IV drug injection promotes clot formation via vascular damage, local infection, or a combination of the two. Malignancy may cause IJ vein thrombosis through local compression and invasion, production of a systemic hypercoagulable state, or both.

Etiology

Thrombosis associated with central venous catheters occurs more frequently than was previously believed. One study found that 66% of patients who had an IJ vein catheter in place at some time during their hospital course had either ultrasonographic or autopsy evidence of IJ thrombus. The frequency was even greater in more critically ill patients, especially those with low cardiac output or shock syndromes.

Causes of IJ thrombosis include the following:

  • Central venous or Swan-Ganz catheters in the IJ vein
  • Central venous or Swan-Ganz catheters in the subclavian vein
  • Individuals who abuse IV drugs using the IJ vein for access
  • Lemierre syndrome
  • Necrotizing soft-tissue infections
  • Neck dissection surgical complications
  • Head and neck malignancy
  • Distant malignancy producing a hypercoagulable state
  • Hypercoagulable state secondary to factor V Leiden, protein C, protein S, or antithrombin III deficiency
  • Jugular bulb catheters
  • Any neck surgery involving prolonged retraction of the IJ vein
  • Trauma
  • Association with ovulation induction with gonadotropins
  • Hyperhomocysteinemia
  • Neck massage
  • Polycythemia
  • Spontaneous causes (often secondary to an undiagnosed malignancy or hypercoagulable state)

Gram-positive organisms that often have high-grade resistance to beta-lactam antibiotics frequently cause septic thrombophlebitis associated with central venous catheters. One study reported a 40% incidence of beta-lactam–resistant organisms with catheter-induced IJ vein thrombosis. Individuals who abuse IV drugs have a very high risk of septic thrombophlebitis caused by methicillin-resistant Staphylococcus aureus (MRSA).

In cases of Lemierre syndrome, anaerobic organisms often predominate. Fusobacterium species (eg, F nucleatum, F necrophorum) are anaerobic gram-negative rods that are often mistaken for Bacteroides species. F necrophorum is the most virulent and commonly isolated pathogen.[2] Other organisms include Bacteroides and Peptostreptococcus species, Eikenella corrodens, and S aureus.

Epidemiology

Some studies suggest that the rate of thrombosis may be lower for Silastic (Dow Corning, Midland, MI) hemodialysis catheters inserted percutaneously than for those inserted surgically. Additionally, the rate of thrombosis may be lower in patients undergoing hemodialysis than in other critically ill patients.

The incidence of Lemierre syndrome has fallen dramatically since the use of antibiotics began in the late 1950s. However, this syndrome still occurs, particularly in underserved populations.

Case series have described IJ vein thrombosis rates of 25-30% after functional neck dissection and hemodialysis catheter placement. However, a significant percentage of affected patients have been advised to undergo recanalization, with excellent long-term patency rates.

The frequency of IJ vein thrombosis in individuals who abuse IV drugs is not known, but this condition usually occurs in people who have been using injectable drugs for years and have exhausted all peripheral access sites.

Prognosis

The outcome is generally good, but with morbidity and mortality similar to those for subclavian and axillary vein thrombosis. PE can occur but is uncommon when full-strength systemic anticoagulation is in place. The incidence of PE is 0.5% for isolated IJ vein thrombosis and 2.4% for combined IJ vein and subclavian/axillary vein thrombosis. Mortality has been reported to be 14% at 1 month, 33% at 3 months, and 42% at 12 months.[3]

Before the antibiotic era, Lemierre syndrome was associated with a mortality exceeding 50%. Today, however, death is uncommon when the syndrome is recognized early and treated with appropriate aggressive medical and surgical therapy. In one series of patients with septic thrombophlebitis occurring over a 9-year period, death occurred in 17% of patients.

Many patients have ongoing critical illness, often with multisystem involvement. This makes it difficult to determine how much the thrombus itself is contributing to mortality. The advantage of being aware of the diagnosis is that the physician can be more vigilant for potential complications and perhaps treat them earlier.

 

Presentation

History and Physical Examination

The symptoms and signs of internal jugular (IJ) vein thrombosis are often very subtle, making it easy to overlook the diagnosis. Pain and swelling at the angle of the jaw and a palpable cord beneath the sternocleidomastoid both may be absent in a minority of patients. Once infection has set in, other objective findings may be found. The following clinical manifestations have been described[4] :

  • Fever (83%)
  • Leukocytosis (78%)
  • Mass or neck swelling (72%)
  • Cervical pain (66%)
  • Cord sign (39%)
  • Sepsis syndrome (39%)
  • Pleuropulmonary complications (28%)
  • Superior vena cava syndrome (11%)
  • Chylothorax (5%)
  • Jugular foramen syndrome (6%)
  • Increased intracranial pressure with symptoms that include headache, visual disturbances, and altered sensorium (rare) [5]

Complications

Once the diagnosis is made, vigilance should be maintained for the following complications:

  • Pulmonary embolism (PE)
  • Subclavian vein thrombosis
  • Superior sagittal sinus thrombosis
  • Superior vena cava syndrome
  • Idiopathic intracranial hypertension (IIH; also referred to as benign intracranial hypertension or pseudotumor cerebri)
  • Laryngeal and lower-airway edema

Infected thrombophlebitis has the following complications:

  • Systemic sepsis syndrome
  • Septic emboli to lungs, liver, spleen, brain, skin, muscle, and bone marrow
  • Empyema
  • Septic arthritis
  • Renal failure
  • Hepatic dysfunction
  • Cerebral edema
 

Workup

Approach Considerations

Often, the cause of internal jugular (IJ) vein thrombosis is obvious (eg, an indwelling catheter). However, some cases call for a more in-depth investigation of the coagulation system or a more extensive search for the cause of a hypercoagulable state. Therefore, the use of laboratory studies must be individualized. Currently available assays detect only 10-20% of inherited hypercoagulable states.

Imaging studies that may be helpful include ultrasonography, computed tomography (CT) with contrast, magnetic resonance imaging (MRI), and nuclear medicine scanning.

Laboratory Studies

The following deficiencies and syndromes can predispose to intravascular thrombosis:

  • Protein C or S deficiency
  • Heparin-induced thrombocytopenia and thrombosis syndrome caused by an antiheparin antibody
  • Lupus anticoagulant/antiphospholipid syndrome
  • Resistance to activated protein C (factor V Leiden)
  • Hyperhomocysteinemia
  • Prothrombin G20210 polymorphism
  • Defective fibrinolysis
  • Dysfibrinogenemia
  • Lipoprotein abnormality
  • Abnormal platelet aggregation
  • Elevated factor VIII, factor IX, factor XI, and antithrombin III

Often a family history or past episodes of arterial thrombosis are present.

Tests for these conditions are generally sent to a reference laboratory, requiring days to return. Warfarin therapy invalidates some of the results of these assays. They are not routinely recommended in all cases, but they should be ordered as clinically indicated.

When disseminated intravascular coagulation (DIC) is suspected on the basis of the clinical presentation, a DIC screen (ie, prothrombin time [PT], activated partial thromboplastin time [aPTT], fibrin split products, and fibrinogen) should be ordered.

Despite the significant interest in the use of a simple blood test to diagnose intravascular thrombosis, no single test currently suffices. Several published studies suggest that D-dimer results have high sensitivity and specificity for intravascular thrombosis. Caution is required in working with currently available commercial test kits. The vast majority of kits now in use in hospitals lack the diagnostic accuracy of the more sophisticated assays used in the small number of published studies.

In cases of suspected septic thrombophlebitis, sending blood cultures in an attempt to isolate the pathogenic organism is critical. Persistently positive blood culture findings are strongly suggestive of an intravascular infection, with the major differential being between a septic thrombophlebitis and endocarditis. Endocarditis can usually be identified by means of transthoracic or transesophageal echocardiography.

Ultrasonography

Ultrasonography is a safe, noninvasive, portable, and widely available test. Venous duplex ultrasonography is the first diagnostic test of choice for many with IJ vein thrombosis. Ultrasonographic findings include a dilated and incompressible vein, intraluminal clot (a late finding), and no response to the Valsalva maneuver (expected change in intraluminal volume secondary to enhanced venous return).

Ultrasonography provides very poor images beneath the clavicle and under the mandible. Doppler ultrasonography may be useful for detecting flow changes secondary to thrombus during the acute phase of clot formation.

Radiography and Computed Tomography

In the past, contrast venography was the criterion standard for confirming a diagnosis of IJ vein thrombosis. However, venography has a number of drawbacks, including exposure to contrast dye and potential dislodgment of clot, with subsequent pulmonary embolism (PE).

Contrast-enhanced CT may be useful for diagnosing suspected IJ vein thrombosis.[6] CT findings include low-density intraluminal thrombus, a sharply defined bright vessel wall (because of contrast uptake by the vasa vasorum), soft-tissue swelling surrounding the IJ vein, and a distended IJ vein proximal to the thrombus.

Other Studies

MRI provides greater soft-tissue contrast and sensitivity to blood flow rates than CT does, and it has the additional advantage of not requiring exposure to intravenous contrast or radiation. However, the examination is usually performed in a distant hospital location and thus is difficult and inconvenient in critically ill patients.

Nuclear medicine tests such as gallium-67 studies have unacceptably high false-positive rates, especially in patients with active malignancies. Study times often are long, and the testing must be performed in the nuclear medicine area; these are distinct disadvantages for critically ill patients.

An IJ vein clot associated with an indwelling catheter, whether located in the IJ vein or the subclavian vein, mandates culture of the catheter (after removal) to rule out infection.

 

Treatment

Approach Considerations

Uncomplicated cases of internal jugular (IJ) vein thrombosis seldom require surgical intervention. Pharmacologic therapy may involve anticoagulants, thrombolytics, or antibiotics as indicated.[7]

Rare indications for a superior vena cava (SVC) filter are similar to those of deep vein thrombosis (DVT) in the lower extremity when upper-extremity DVT is associated with an IJ vein thrombosis. These include the clinical setting of pulmonary embolism (PE) in which therapeutic anticoagulation has failed or is contraindicated. The contraindications for surgery are few but would include uncorrected coagulopathy and cardiac risks for the procedure that are believed to outweigh the benefits.

Pharmacologic Therapy

Once a diagnosis of IJ vein thrombosis is made, consideration should be given to initiating anticoagulant therapy. To date, unfortunately, there have been no studies of sufficient size to guide physicians in this area. Clearly, many patients do well without serious effects, as evidenced by the frequency with which IJ vein thrombosis is underdiagnosed.

The true risk of PE is unknown. The most commonly quoted rate of PE occurring in the setting of IJ thrombosis is 5%; however, this statistic is taken from a relatively small retrospective study performed more than 25 years ago. A later retrospective study demonstrated PE rates of 0.5% and 2.4% for isolated IJ vein thrombosis and combined subclavian/axillary vein and IJ vein thrombosis, respectively.

Isolated case series have described the use of thrombolytic therapy in this setting, usually via catheters inserted directly adjacent to the thrombus. Most reports involved patients with extensive thrombus extending into the sigmoid sinus, in whom treatment caused few complications. However, neither the indications for nor the safety of thrombolytic treatment has been defined.

If an indwelling catheter is present, it should be removed. Exceptions to this policy are rare but include situations where no other options for venous access exist in a patient who would experience a life-threatening situation without it. When the indwelling catheter cannot be removed, the use of unfractionated heparin or low-molecular-weight heparin is recommended in the acute setting to prevent central propagation or symptomatic PE and to maintain any restored venous patency.[8]

In the setting of infection, many patients do well when given antibiotics alone, without anticoagulant therapy. However, in the presence of septic emboli or with clear evidence of clot propagation, many physicians choose to add systemic anticoagulation. The major risk involves further bleeding and even airway compromise from expanding hematoma, especially in association with central venous catheters.

In the setting of thrombophlebitis associated with central venous catheters, antibiotic therapy directed at gram-positive organisms should be promptly instituted. Vancomycin is a good initial choice and can be changed to nafcillin if culture data subsequently indicate sensitivity to methicillin. Daptomycin has also been approved for use in this setting.

In all other cases of infected IJ vein thrombus, prolonged antibiotic therapy specifically directed against anaerobic organisms should be promptly instituted as soon as blood cultures are obtained. Recommended antibiotics include ticarcillin-clavulanate and ampicillin-sulbactam. In patients with true anaphylaxis to penicillin, clindamycin, metronidazole, or chloramphenicol could be used as alternatives. For all cases of thrombophlebitis, therapy should be continued for 4-6 weeks.

Surgical Intervention

Although surgical intervention is rarely necessary for uncomplicated cases, IJ vein thrombosis associated with a deep neck infection calls for drainage of any fluid collections and debridement of all infected tissue. Likewise, extensive and complete debridement is warranted for cervical necrotizing fasciitis.

In patients with intraluminal abscesses, excision of the IJ vein may be required to prevent subsequent serious complications. However, most cases of postanginal sepsis can be managed medically, without the need for resection of the infected vein. Cases that do not respond to antibiotic therapy are unusual; it is important to remember that fever may persist for some time, especially in cases of metastatic infection.

The carotid sheath often protects the carotid artery. However, if this structure becomes involved, early and prompt surgical intervention is required to prevent devastating neurologic or airway complications.

Placement of superior vena cava filter

Indications for a Greenfield SVC filter are rare. No reports demonstrate the use of an SVC filter for an isolated IJ vein thrombosis. Indications for an SVC filter with axillary/subclavian vein thrombosis are similar to those of lower-extremity DVT, including upper-extremity DVT that extended to the IJ vein. Therefore, in the clinical setting of an axillary/subclavian vein thrombosis alone or combined with an IJ vein thrombus with PE in which therapeutic anticoagulation has failed or is contraindicated, an SVC filter should be inserted.

Before filter placement, superior vena cavograms are obtained in all patients to determine caval size and to exclude venous abnormalities and SVC thrombus.[9] Whenever possible, the filter is placed via the right common femoral vein. Placement is more difficult in the SVC than in the inferior vena cava (IVC) because the area for appropriate placement is smaller. For femoral vein insertion, a jugular insertion kit is used to facilitate orientation; for jugular vein insertion, a femoral insertion kit is used.

After the procedure, a chest radiograph should be obtained to assess for filter migration, dislodgment, or fracture.

 

Medication

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Anticoagulants, Hematologic

Class Summary

Anticoagulant medications prevent further clot deposition. They allow the natural fibrinolytic mechanisms to lyse the existing clot.

Heparin

Heparin augments the activity of antithrombin III and prevents conversion of fibrinogen to fibrin. It does not actively lyse but is able to inhibit further thrombogenesis. The drug prevents the reaccumulation of clot after spontaneous fibrinolysis.

Warfarin (Coumadin, Jantoven)

Warfarin interferes with the hepatic synthesis of vitamin K–dependent coagulation factors. It is used for prophylaxis and treatment of venous thrombosis, pulmonary embolism (PE), and thromboembolic disorders. Tailor the dose to maintain an international normalized ratio (INR) in the range of 2.0-3.0.

Thrombolytic Agents

Class Summary

As advanced by the American College of Chest Physicians in their fourth consensus conference on antithrombotic therapy, thrombolytic treatment is indicated for acute, massive PE with hemodynamic instability in patients who do not seem prone to bleeding. These agents dissolve recent clots promptly by activating a plasma proenzyme, plasminogen, to its active form, plasmin. Plasmin degrades fibrin to soluble peptides.

Thrombolytic therapy speeds pulmonary tissue reperfusion and rapidly reverses right-sided heart failure. It improves pulmonary capillary blood flow and more rapidly improves hemodynamic parameters.

Reteplase

Reteplase is used in the management of PE in hemodynamically unstable patients. Its safety and efficacy with concomitant administration of heparin or aspirin during the first 24 hours after symptom onset have not been investigated.

Tenecteplase (TNKase)

Tenecteplase is a modified version of alteplase that is made by substituting three amino acids. It has a longer half-life than alteplase and thus can be given as a single bolus infused over 5 seconds (as opposed to the 90 minutes required for alteplase). It appears to cause less nonintracranial bleeding than alteplase but carries a comparable risk of intracranial bleeding and stroke.

Base the dose on the patient's weight. Initiate treatment as soon as possible after the onset of acute myocardial infarction symptoms. Because tenecteplase contains no antibacterial preservatives, it must be reconstituted immediately before use.

Alteplase (Activase)

Alteplase, or tissue plasminogen activator (tPA), exerts an effect on the fibrinolytic system to convert plasminogen to plasmin. Plasmin degrades fibrin, fibrinogen, and procoagulant factors V and VIII. The serum half-life of alteplase is 4-6 minutes but is lengthened when the drug is bound to fibrin in clot.

Antibiotics

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. For all cases of thrombophlebitis, therapy should be continued for 4-6 weeks.

Nafcillin (Nallpen in Dextrose)

Nafcillin is used in the initial therapy for suspected penicillin G–resistant streptococcal or staphylococcal infections. Parenteral therapy should be used initially in severe infections, with a change made to oral treatment as the condition warrants.

Because of thrombophlebitis, particularly in elderly persons, nafcillin should be administered parenterally only for a short term (1-2 days); change to an oral antibiotic should be made as clinically indicated.

Vancomycin

Vancomycin is a potent antibiotic directed against gram-positive organisms and active against Enterococcus species. To avoid toxicity, the current recommendation is to assay vancomycin trough levels after the third dose, drawn 0.5 hour prior to the next dosing. Use creatinine clearance to adjust the dose in patients diagnosed with renal impairment.

Vancomycin is used in conjunction with gentamicin for prophylaxis in penicillin-allergic patients undergoing gastrointestinal or genitourinary procedures.

Daptomycin (Cubicin)

Daptomycin binds to bacterial membranes and causes rapid membrane potential depolarization, thereby inhibiting protein, DNA, and RNA synthesis, ultimately causing cell death. It is indicated for complicated skin and skin-structure infections caused by Staphylococcus aureus (including methicillin-resistant strains), Streptococcus pyogenes, Streptococcus agalactiae, Streptococcus dysgalactiae, and Enterococcus faecalis (vancomycin-susceptible strains only).

Ampicillin and sulbactam (Unasyn)

This agent features ampicillin combined with a beta-lactamase inhibitor. It interferes with bacterial cell-wall synthesis during active replication, causing bactericidal activity against susceptible organisms.

Chloramphenicol

Chloramphenicol binds to 50 S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. It is effective against gram-negative and gram-positive bacteria. The oral form is not available in the United States.

Clindamycin (Cleocin)

This agent is a semisynthetic antibiotic produced by 7(S)-chloro-substitution of the 7(R)-hydroxyl group of the parent compound, lincomycin. Clindamycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl transfer ribonucleic acid (tRNA) from ribosomes, causing RNA-dependent protein synthesis to arrest. The drug is widely distributed in the body without penetration of the central nervous system (CNS). It is protein-bound and excreted by the liver and kidneys.

Penicillin G aqueous (Pfizerpen)

Penicillin G interferes with the synthesis of cell-wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.

Metronidazole (Flagyl)

Metronidazole is an imidazole ring–based antibiotic active against various anaerobic bacteria and protozoa. It is used in combination with other antimicrobial agents.

Ticarcillin and clavulanate potassium (Timentin)

This drug combination inhibits the biosynthesis of cell-wall mucopeptide and is effective during the stage of active growth. It consists of an antipseudomonal penicillin plus a beta-lactamase inhibitor and provides coverage against most gram-positives, most gram-negatives, and most anaerobes.

 

Questions & Answers

Overview

What is internal jugular (IJ) vein thrombosis?

What anatomy is relevant to internal jugular (IJ) vein thrombosis?

What is Virchow’s triad?

What is the pathophysiology of internal jugular (IJ) vein thrombosis?

What is the prevalence of a central venous catheter etiology for internal jugular (IJ) vein thrombosis?

What causes internal jugular (IJ) vein thrombosis?

What is the role pathogens in the etiology of internal jugular (IJ) vein thrombosis?

What is the incidence of internal jugular (IJ) vein thrombosis?

What is the prognosis of internal jugular (IJ) vein thrombosis?

Presentation

What are the symptoms and signs of internal jugular (IJ) vein thrombosis?

What are complications of internal jugular (IJ) vein thrombosis?

What are the complications of Lemierre syndrome?

Workup

Which studies should be performed in the workup of internal jugular (IJ) vein thrombosis?

Which deficiencies and syndromes suggest intravascular internal jugular (IJ) vein thrombosis?

How does warfarin affect lab testing for internal jugular (IJ) vein thrombosis?

Which tests should be performed in the evaluation of internal jugular (IJ) vein thrombosis if disseminated intravascular coagulation (DIC) is suspected?

Which tests should be performed in the evaluation of internal jugular (IJ) vein thrombosis if septic thrombophlebitis (Lemierre syndrome) is suspected?

What is the role of ultrasonography in the diagnosis of internal jugular (IJ) vein thrombosis?

What is the role of contrast venography in the diagnosis of internal jugular (IJ) vein thrombosis?

What is the role of contrast venography CT scanning in the diagnosis of internal jugular (IJ) vein thrombosis?

What is the role of MRI in diagnosis of internal jugular (IJ) vein thrombosis?

What is the role of nuclear medicine in diagnosis of internal jugular (IJ) vein thrombosis?

Treatment

What are the treatment options for internal jugular (IJ) vein thrombosis?

What is the role of pharmacologic therapy in the treatment of internal jugular (IJ) vein thrombosis?

How is internal jugular (IJ) vein thrombosis treated when an indwelling catheter cannot be removed?

What are the treatment options for internal jugular (IJ) vein thrombosis when infection is present?

What is the role of surgery in the treatment of internal jugular (IJ) vein thrombosis?

What is the role of a superior vena cava (SVC) filter in the treatment of internal jugular (IJ) vein thrombosis?

Medications

What is the goal of drug treatment for internal jugular (IJ) vein thrombosis?