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Internal Jugular Vein Thrombosis

  • Author: Dale K Mueller, MD; Chief Editor: Vincent Lopez Rowe, MD  more...
 
Updated: Jul 20, 2016
 

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). 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.

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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.

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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.

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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
  • Deep neck infections
  • 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.[1] Other organisms include Bacteroides and Peptostreptococcus species, Eikenella corrodens, and S aureus.

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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.

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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.[2]

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.

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Contributor Information and Disclosures
Author

Dale K Mueller, MD Co-Medical Director of Thoracic Center of Excellence, Chairman, Department of Cardiovascular Medicine and Surgery, OSF Saint Francis Medical Center; Cardiovascular and Thoracic Surgeon, HeartCare Midwest, Ltd, A Subsidiary of OSF Saint Francis Medical Center; Section Chief, Department of Surgery, University of Illinois at Peoria College of Medicine

Dale K Mueller, MD is a member of the following medical societies: American College of Chest Physicians, American College of Surgeons, American Medical Association, Chicago Medical Society, Illinois State Medical Society, International Society for Heart and Lung Transplantation, Society of Thoracic Surgeons, Rush Surgical Society

Disclosure: Received consulting fee from Provation Medical for writing.

Coauthor(s)

Michael J Dacey, MD Consulting Staff, Department of Internal Medicine, Division of Critical Care, Kent County Hospital

Disclosure: Nothing to disclose.

Chief Editor

Vincent Lopez Rowe, MD Professor of Surgery, Program Director, Vascular Surgery Residency, Department of Surgery, Division of Vascular Surgery, Keck School of Medicine of the University of Southern California

Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, Society for Vascular Surgery, Vascular and Endovascular Surgery Society, Society for Clinical Vascular Surgery, Pacific Coast Surgical Association, Western Vascular Society

Disclosure: Nothing to disclose.

Acknowledgements

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
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  2. Ascher E, Salles-Cunha S, Hingorani A. Morbidity and mortality associated with internal jugular vein thromboses. Vasc Endovascular Surg. 2005 Jul-Aug. 39 (4):335-9. [Medline].

  3. Tovi F, Fliss DM, Gatot A, Hertzanu Y. Septic jugular thrombosis with abscess formation. Ann Otol Rhinol Laryngol. 1991 Aug. 100(8):682-4. [Medline].

  4. Fuhrman T, Balatbat J, Frakes J, Metz R. Internal jugular thrombosis causing increased intracranial pressure and upper airway edema. Internet J Anesthesiol. 1999. 4 (3):1-5. [Full Text].

  5. Kim BY, Yoon DY, Kim HC, Kim ES, Baek S, Lim KJ, et al. Thrombophlebitis of the internal jugular vein (Lemierre syndrome): clinical and CT findings. Acta Radiol. 2013 Jul. 54(6):622-7. [Medline].

  6. Sheikh MA, Topoulos AP, Deitcher SR. Isolated internal jugular vein thrombosis: risk factors and natural history. Vasc Med. 2002 Aug. 7 (3):177-9. [Medline]. [Full Text].

  7. 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. 1999 Jan. 210(1):53-8. [Medline].

 
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