Given the widespread use of CVADs, the prevalence of head and neck surgery, and the increased use of transvenous medical devices, iatrogenic sources are the most common causes of JVT in modern medicine [8–10]. IJV occlusion (typically non-thrombotic) is infrequently seen postoperatively following head and neck surgery (Figs. 8–15). Among iatrogenic causes, the vast majority of JVT is due to central venous catheters, often resulting in “uphill thrombosis” that propagates into the IJV from the downstream subclavian or brachiocephalic veins (Fig. 16). At-risk patient populations include those with chronic indwelling central venous catheters, as might be utilized for chemotherapy or frequent blood draws, and critically ill neonates requiring central venous access. JVT as a complication of other transvenous biomedical devices, such as cardioverter defibrillators, pacemakers, and ventriculoatrial shunts, is seen less commonly but has been reported in the medical literature [9, 10]. As previously described, most iatrogenic causes of JVT center around catheter-/device-induced venous stasis and endothelial injury, although it is important to consider superimposed hypercoagulability in these typically ill patients.

A large group of patients with increased susceptibility to iatrogenic JVT is hemodialysis (HD) patients, as they tend to have numerous, long-term CVADs placed over a lifetime (Fig. 17). Studies have demonstrated that in HD patients, JVT risk increases with both duration of catheter placement and total lifetime number of catheters placed, with subsequent JVT reported in 2–64 % of cases based on older studies [8, 11]. The underlying renal insufficiency itself is associated with hemostatic abnormalities, and HD adds to these disturbances with turbulent flow, high shear stress, and contact of blood to artificial surfaces. This leads to activation of the coagulation cascade, which is the target of anticoagulation agents, such as unfractionated heparin and low-molecular-weight heparin.

Another subset of patients at risk for IJV thrombosis or occlusion is that group who has undergone neck surgery, most commonly following neck dissection for head and neck cancer. While IJV patency is dependent on the type and extent of neck dissection (with intentional sacrifice of the IJV performed in some cases), true thrombosis or complete occlusion following IJV-sparing neck dissection is uncommon [12]. However, a diminution in IJV caliber is expected following neck dissection, reaching a nadir in the immediate postoperative period and frequently returning to near-normal caliber by 3 months [12]. Uncommonly, JVT can be seen following carotid endarterectomy, presumably due to prolonged intraoperative retraction of the IJV.

Lastly, there are reports of JVT following cervical manipulation, including chiropractic and deep tissue massage. Other than case reports, the literature evidence for or against cervical manipulation-induced IJV thrombosis is certainly lacking. The mechanism of thrombus formation in these rare cases is not well elucidated, although it might theoretically reflect a combination of pressure-induced venous stasis and traumatic endothelial injury.

Like lower extremity deep vein thrombosis (DVT), JVT is commonly associated with malignancy, with coincidence reported up to 10–35 % in some series [7, 13] (Figs. 18–21). Mechanistically, neoplasm-related thrombosis of the IJV results from (a) compression/invasion of the vessel lumen by lymphadenopathy or primary tumor, resulting in static blood flow, (b) a complex, incompletely understood cancer-induced hypercoagulable state (often referred to as migratory thrombophlebitis or Trousseau syndrome) that results in increased levels or activity of several procoagulant factors (including tissue factor, fibrinogen, factor VIIa, factor VIII, factor IXa, factor Xa, C-reactive protein, carcinoma mucins, tumor-associated cysteine proteinase, or oncogene activation), or (c) iatrogenic consequences of cancer treatment (cf. Iatrogenic) [4, 14, 15].

Among all cancer patients, treatment-related causes are the most common etiology of JVT; these include CVADs, prolonged immobility, intravascular administration of caustic chemotherapeutic agents, postsurgical vascular injury, and postradiation therapy vascular complications. Nonetheless, the presence of JVT, especially in cancer patients, should prompt the interpreting radiologist to carefully assess the cervical lymph node stations for metastatic lymphadenopathy and to assess the deep spaces of the neck for a lesion exerting mass effect on the thrombosed IJV. While most often due to underlying head and neck cancer (such as squamous cell carcinoma of the aerodigestive tract or thyroid malignancy), cervical chain lymphadenopathy causing JVT can also be seen in widely disseminated metastatic disease of any number of primary malignancies [16–18]. The most common of these primary malignancies include pancreatic, lung, stomach, and ovarian cancer, which may contribute to JVT due to increased factor VIII and thromboplastin levels. Additionally, nonmalignant neoplasms, such as lymphangioleiomyomatosis, can lead to JVT due to local mass effect and resulting venous stasis. Both contrast-enhanced CT (CECT) and ultrasound (US) are useful modalities for assessment of the neck masses, with US offering the opportunity for image-guided fine needle aspiration or core needle biopsy of suspicious masses or lymphadenopathy.

Prior to the widespread use of antibiotics in the 1940s, infection was by far the most common etiology of JVT. However, in current medical practice infectious sources of JVT are quite rare, attributed mainly to IVDA (Figs. 22–24) and sporadic cases of typically oropharyngeal infections resulting in Lemierre syndrome. IVDA increases the risk of JVT for several reasons: (1) shooters typically do not employ sterile technique, thus risking blood-borne infection; (2) traumatic endothelial injury from the needle encourages thrombosis; (3) infectious (mycotic) endothelial damage by blood-borne organisms results in prothrombotic infiltration and congestion of the adventitia (and subsequently the other layers of the vein wall) by inflammatory cells; and (4) IVDA-associated deep neck infection contributes to altered blood flow dynamics, including venous stasis [19]. Other infectious causes of the deep spaces of the head and neck, such as postsurgical infection (Figs. 25–33), acute otomastoiditis, or postauricular abscess, may also contribute to the development of JVT, albeit much less commonly. Additionally, an increased risk of JVT in immunocompetent patients with severe acute cytomegalovirus infection has been described, a link which may be under-recognized and underreported.