AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Thrombosis of the internal jugular (IJ) vein 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 drug abuse. It is also reported to occur spontaneously. IJ thrombosis itself can have serious potentially life-threatening complications that include systemic sepsis, chylothorax, papilledema, airway edema, and pulmonary embolism. The diagnosis often is very challenging and requires, first and foremost, a high degree of clinical suspicion.

History of the Procedure

At the turn of the 20th century, thrombosis of the IJ vein was a feared complication of acute oropharyngeal infection. In 1936, Lemierre described the first case series of septic thrombophlebitis of the IJ vein, often complicated by metastatic infection.¹ The diagnosis was intuitive, although before the advent of effective antibiotic therapy, little could be offered and more than 50% of patients died.

Today, with widespread use of the IJ vein for venous access, central venous catheters now are the most common underlying cause of IJ thrombosis. Of concern is a recent trend in increasing number of individuals who abuse intravenous drugs who present with IJ thrombosis secondary to repeated drug injection directly into the IJ vein. Other causes include local malignancy and head, neck, and cardiac surgery. Rare causes include polycythemia, hyperhomocysteinemia, and neck massage.

Problem

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.

The thrombosis may become secondarily infected, producing a 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.

Frequency

Some studies suggest that the rate of thrombosis may be lower for percutaneously inserted silastic hemodialysis catheters compared to those inserted surgically. Additionally, the rate of thrombosis may be lower in patients undergoing hemodialysis compared with other critically ill patients.

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

Recent case series describe IJ thrombosis rates of 25-30% following functional neck dissection and hemodialysis catheter placement. However, a significant percentage of affected patients have been suggested to undergo recanalization, with excellent long-term patency rates.

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

Etiology

Thrombosis associated with central venous catheters occurs more frequently than 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.

The 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 intravenous drugs using the IJ vein for access
• Lemierre syndrome
• Deep neck infections
• Necrotizing soft tissue infections
• Neck dissection surgery complication
• Head and neck malignancy
• Distant malignancy producing 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 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 thrombosis. Individuals who abuse intravenous drugs have a very high risk of septic thrombophlebitis caused by methicillin-resistant strains of Staphylococcus aureus.

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. Other organisms include Bacteroides and Peptostreptococcus species and Eikenella corrodens.

Pathophysiology

The classic triad predisposing to intravascular thrombosis was described first by Virchow and includes blood vessel trauma, stasis of blood flow, and a 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, including odontogenic infections and infections of the tonsils, peritonsillar tissue, pharynx, sinuses, middle ear, and parotids, all 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 lymphatics. Subsequent sepsis syndrome may occur, usually a week or more after the primary infection.

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

Intravenous drug injection promotes clot formation via vascular damage, local infection, or a combination of both. Malignancy may cause IJ thrombosis via local compression and invasion and/or by producing a systemic hypercoagulable state.

Clinical

The symptoms and signs of IJ thrombosis can often be 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 muscle both may be absent in a significant minority of patients. Once infection has set in, other objective findings may be found. Tovi et al described the following clinical manifestations in their 1991 series of patients with septic IJ thrombosis as follows:²

Clinical manifestations of IJ thrombosis occur in the following percentages of patients:

• Fever - 83% of patients
• Leukocytosis - 78% of patients
• Cervical pain - 66% of patients
• Mass or neck swelling - 72% of patients
• Cord sign - 39% of patients
• Sepsis syndrome - 39% of patients
• Pleuropulmonary complications - 28% of patients
• Superior vena cava syndrome - 11% of patients
• Chylothorax - 5% of patients
• Jugular foramen syndrome - 6% of patients
• Increased intracranial pressure with symptoms that include headache, visual disturbances, and altered sensorium - rare³

INDICATIONS

Section 3 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Rare indications for a superior vena cava filter are similar to those of deep venous thrombosis in the lower extremity when an upper extremity deep vein thrombosis is associated with an internal jugular thrombosis. These include a clinical setting of pulmonary embolism in which therapeutic anticoagulation has failed or is contraindicated.

RELEVANT ANATOMY

Section 4 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

The internal jugular (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 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, IJ vein, cranial nerves IX-XII, and lymph nodes.

CONTRAINDICATIONS

Section 5 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

The contraindications to surgery are few but would include uncorrected coagulopathy and cardiac risks for the procedure that are believed to outweigh the benefits.

WORKUP

Section 6 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Lab Studies

• Often, the cause of the internal jugular (IJ) thrombosis is obvious (eg, indwelling catheter). However, some cases require 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.
• Protein C, protein S, 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, abnormal platelet aggregation, elevated factor VIII, factor IX, factor XI, and antithrombin III are as follows:
• • Deficiencies of the coagulation cascade or these syndromes predispose the patient to spontaneous intravascular thrombosis. However, often a family history and/or past episodes of arterial thrombosis are present.
  • These tests are generally sent to a reference laboratory, requiring days to return. Coumadin 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.
• Order a disseminated intravascular coagulation (DIC) screen (ie, prothrombin time [PT], activated partial thromboplastin time [aPTT], fibrin split products, fibrinogen) when DIC is suspected on the basis of clinical presentation.
• D-dimer is as follows:
• • 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.
  • Use caution when working with currently available commercial test kits. The vast majority of kits now in use in hospitals do not have the diagnostic accuracy of the more sophisticated assays used in the small number of published studies.
• Blood cultures are as follows:
• • 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 on transthoracic or transesophageal echocardiography.

Imaging Studies

• Contrast venography
• • In the past, the criterion standard for confirming a diagnosis was contrast venography.
  • Venography has a number of drawbacks, including exposure to contrast dye and potential dislodgement of clot, with subsequent pulmonary embolism.
• Ultrasonography
• • Ultrasonography is a safe, noninvasive, portable, and widely available test that is the test of choice for many with IJ 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.
• Contrast-enhanced CT scanning
• • CT scanning with intravenous contrast is considered by some to be the study of choice for suspected IJ thrombosis.
  • CT scan 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.
• MRI
• • MRI provides greater soft tissue contrast and sensitivity to blood flow rates when compared to CT scanning.
  • It does not require exposure to intravenous contrast or radiation. The examination is usually performed in a distant hospital location, making it difficult and inconvenient in critically ill patients.
• Nuclear medicine scanning
• • 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, both of which are distinct disadvantages for critically ill patients.

Other Tests

• Catheter tip and intradermal culture: IJ clot associated with an indwelling catheter, whether located in the IJ or subclavian vein, mandates culture of the catheter (once removed) to rule out infection.

TREATMENT

Section 7 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Medical therapy

Once a diagnosis of internal jugular (IJ) thrombosis is made, consider the use of anticoagulant therapy. Unfortunately, no studies of sufficient size are currently available to guide physicians in this area. Clearly, many patients do well without serious effects, as evidenced by the fact that the condition is often underdiagnosed.

The risk of pulmonary embolism is truly unknown. The most commonly quoted rate of pulmonary embolism 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 recent retrospective study demonstrated pulmonary embolism rates of 0.5% and 2.4% for isolated IJ thrombosis and combined subclavian/axillary vein and IJ thrombosis, respectively.

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

If an indwelling catheter is present, remove it. Exceptions to this are rare but do include situations where no other options for venous access exist in a patient who would experience a life-threatening situation without it.

In the setting of infection, many patients do well with 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 the expanding hematoma, especially when associated with central venous catheters.

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

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

Surgical therapy

Uncomplicated cases of IJ thrombosis seldom require surgical intervention. However, cases associated with deep neck infections require drainage of any fluid collections and debridement of all infected tissue. Likewise, cervical necrotizing fasciitis requires extensive and complete debridement.

Cases of intraluminal abscesses may require excision of the IJ vein in order 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, and, importantly, remember that fever may persist for some time, especially in cases of metastatic infection.

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

Indications for a superior vena cava (SVC) Greenfield filter are rare. No reports demonstrate the use of a SVC filter for an isolated IJ thrombosis. Indications for a superior vena caval filter with axillary/subclavian vein thrombosis are similar to those of deep venous thrombosis in the lower extremity. These include upper extremity deep vein thrombosis that extended to the IJ. Therefore, in the clinical setting of an axillary/subclavian vein thrombosis alone or combined with an IJ thrombus with a pulmonary embolism in which therapeutic anticoagulation has failed or is contraindicated, a SVC filter should be inserted.

Preoperative details

Superior vena cavograms are obtained in all patients prior to filter placement to determine caval size and to exclude venous abnormalities and SVC thrombus.⁴

Intraoperative details

Whenever possible, the filters are placed via the right common femoral vein. Filter placement in the SVC is more difficult than in the inferior vena cava (IVC) secondary to the relatively small area for appropriate filter placement. For femoral insertion of the SVC filter, a jugular insertion kit is used for correct filter orientation. For jugular vein insertion, a femoral insertion kit is used.

Postoperative details

A chest radiography should be obtained to access for filter migration, dislodgement, or fracture.

Follow-up

For excellent patient education resources, visit eMedicine's Lung and Airway Center and Circulatory Problems Center. Also, see eMedicine's patient education articles Pulmonary Embolism, Venous Access Devices, Phlebitis, and Blood Clot in the Legs.

COMPLICATIONS

Section 8 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Once a diagnosis of internal jugular (IJ) thrombosis is made, be vigilant for the following complications:

• Pulmonary embolism
• Subclavian vein thrombosis
• Superior sagittal sinus thrombosis
• Superior vena cava syndrome
• Pseudotumor cerebri
• Laryngeal and lower airway edema
• Infected thrombophlebitis, which 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

OUTCOME AND PROGNOSIS

Section 9 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Outcome is generally good but has similar morbidity and mortality to subclavian and axillary vein thrombosis. Pulmonary embolism can occur but is uncommon when full-strength systemic anticoagulation is in place. Rates of pulmonary embolism are 0.5% for isolated internal jugular (IJ) thrombosis and 2.4% for combined IJ and subclavian/axillary thrombosis. Mortality rates at 1, 3, and 12 months have been reported to be 14%, 33%, and 42%, respectively.⁵

Lemierre syndrome was associated with a mortality rate of higher than 50% prior to antibiotic use. However, when recognized early and treated with appropriate aggressive medical and surgical therapy, death is uncommon today. 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 the contribution to mortality by the thrombus itself difficult to determine. The advantage of being aware of the diagnosis is that the physician can be more vigilant for potential complications and perhaps treat them earlier.

FUTURE AND CONTROVERSIES

Section 10 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Studies have demonstrated similar morbidity and mortality compared with those of upper extremity deep vein thrombosis; therefore, consideration should be given to treat these 2 entities in a similar fashion. Randomized clinical trials should investigate anticoagulation as primary treatment and superior vena cava filter placement as secondary treatment in the setting of therapeutic anticoagulation that has failed or is contraindicated. Currently, no well-designed clinical trials are available to assess this. If, in fact, the incidence is as high as is suspected now, the question would lend itself well to a randomized controlled clinical trial.

Thrombolytic treatment has rarely been used. Consideration should be given for treatment of IJ thrombosis in the setting of pulmonary embolism with thrombolytics in a randomized clinical trial.

The best method for making the diagnosis once suspicion is raised should also be assessed. A study assessing the merits of CT scanning, MRI, and ultrasonography would not be difficult to perform.

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

1. Lemierre A. On certain septicemias due to anaerobic organisms. Lancet. 1936;1:701-3.
2. Tovi F, Fliss DM, Gatot A, Hertzanu Y. Septic jugular thrombosis with abscess formation. Ann Otol Rhinol Laryngol. Aug 1991;100(8):682-4. [Medline].
3. Fuhrman T, Balatbat J, Frakes J. Internal jugular thrombosis causing increased intracranial pressure and upper airway edema. The internet journal of anesthesiology. 2000;4:[Full Text].
4. Spence LD, Gironta MG, Malde HM, Mickolick CT, Geisinger MA, Dolmatch BL. Acute upper extremity deep venous thrombosis: safety and effectiveness of superior vena caval filters. Radiology. Jan 1999;210(1):53-8. [Medline].
5. Ascher E, Salles-Cunha S, Hingorani A. Morbidity and mortality associated with internal jugular vein thromboses. Vasc Endovascular Surg. Jul-Aug 2005;39(4):335-9.
6. Agraharkar M, Isaacson S, Mendelssohn D, et al. Percutaneously inserted silastic jugular hemodialysis catheters seldom cause jugular vein thrombosis. ASAIO J. Apr-Jun 1995;41(2):169-72. [Medline].
7. Ahmed N, ALIA. Thrombosis after central venous cannulation. Med J Aust. Feb 21 1976;1(8):217-20. [Medline].
8. Albertyn LE, Alcock MK. Diagnosis of internal jugular vein thrombosis. Radiology. Feb 1987;162(2):505-8.
9. Carpenter JP, Holland GA, Baum RA, et al. Magnetic resonance venography for the detection of deep venous thrombosis: comparison with contrast venography and duplex Doppler ultrasonography. J Vasc Surg. Nov 1993;18(5):734-41. [Medline].
10. Chastre J, Cornud F, Bouchama A, et al. Thrombosis as a complication of pulmonary-artery catheterization via the internal jugular vein: prospective evaluation by phlebography. N Engl J Med. Feb 4 1982;306(5):278-81. [Medline].
11. Chowdhury K, Bloom J, Black MJ, al-Noury K. Spontaneous and nonspontaneous internal jugular vein thrombosis. Head Neck. Mar-Apr 1990;12(2):168-73. [Medline].
12. Coplin WM, O'Keefe GE, Grady MS, et al. Thrombotic, infectious, and procedural complications of the jugular bulb catheter in the intensive care unit. Neurosurgery. Jul 1997;41(1):101-7; discussion 107-9. [Medline].
13. Cosgrove EF, Colodny SM, Pesce RR. Adult respiratory distress syndrome as a complication of postanginal sepsis. Chest. May 1993;103(5):1628-9. [Medline].
14. Gurley MB, King TS, Tsai FY. Sigmoid sinus thrombosis associated with internal jugular venous occlusion: direct thrombolytic treatment. J Endovasc Surg. Aug 1996;3(3):306-14. [Medline].
15. Hubsch PJ, Stiglbauer RL, Schwaighofer BW, et al. Internal jugular and subclavian vein thrombosis caused by central venous catheters. Evaluation using Doppler blood flow imaging. J Ultrasound Med. Nov 1988;7(11):629-36. [Medline].
16. Karnik R, Valentin A, Winkler WB, et al. Duplex sonographic detection of internal jugular venous thrombosis after removal of central venous catheters. Clin Cardiol. Jan 1993;16(1):26-9. [Medline].
17. Kroger K, Gocke C, Schelo C, et al. Association of subclavian and jugular vein thrombosis: color doppler sonographic evaluation. Angiology. Mar 1998;49(3):189-91. [Medline].
18. Larkey D, Williams CR, Fanning J, et al. Fatal superior sagittal sinus thrombosis associated with internal jugular vein catheterization. Am J Obstet Gynecol. Dec 1993;169(6):1612-4. [Medline].
19. Leontsinis TG, Currie AR, Mannell A. Internal jugular vein thrombosis following functional neck dissection. Laryngoscope. Feb 1995;105(2):169-74. [Medline].
20. Myers EM, Kirkland LS Jr, Mickey R. The head and neck sequelae of cervical intravenous drug abuse. Laryngoscope. Feb 1988;98(2):213-8. [Medline].
21. Scaramella JG. Hyperhomocysteinemia and left internal jugular vein thrombosis with Ménière's symptom complex. Ear Nose Throat J. Nov 2003;82(11):856, 859-60, 865. [Medline].
22. Wada Y, Yanagihara C, Nishimura Y. Internal jugular vein thrombosis associated with shiatsu massage of the neck. J Neurol Neurosurg Psychiatry. Jan 2005;76(1):142-3. [Medline].
23. Wilkin TD, Kraus MA, Lane KA, Trerotola SO. Internal jugular vein thrombosis associated with hemodialysis catheters. Radiology. Sep 2003;228(3):697-700. [Medline].

Article Last Updated: Mar 12, 2008