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Background
Septic thrombophlebitis (ST) is an important vascular complication of infection and inflammation resulting from direct extension or venolymphatic drainage of an infected area that propagates. Endothelial damage, venous stasis, and hypercoagulability may play a role. Treatment depends on location and source of infection, but includes antibiotics and often anticoagulation.

Educational Goals / Teaching Points
Postpharyngitis ST of the internal jugular vein is known as Lemierre syndrome (LS), classically caused by an anaerobe gram negative bacillus, Fusobacterium necrophorum affecting otherwise healthy young adults several weeks after primary infection. LS has expanded to include additional pathogens with polymicrobial bacteremia in more than 1/3 of patients. Additional sources include odontogenic infection, sinusitis, mastoiditis, otitis media, and parotitis. Pylephlebitis is ST of the portal vein. Diverticulitis is the most common inciting infection in more than 1/3 of patients. Tributaries such as the superior mesenteric vein are implicated in up to 42% of cases. Bowel ischemia, infarction, and death have been reported with mesenteric vein involvement. Fever, abdominal pain, and hepatomegaly may be present. Jaundice is unusual without cholangitis or hepatic abscesses, which have been reported in up to 37% of cases. Portal hypertension can result as a long-term complication. Pelvic ST is a gynecologic complication occurring postpartum or in association with pelvic surgery, pelvic inflammatory disease, or underlying malignancy. Blood cultures may be negative. Two clinical syndromes have been described, which include ovarian vein thrombophlebitis (OVT) and deep septic pelvic thrombophlebitis (DSPT). OVT commonly presents with fever and pain 1 week after delivery or surgery and can be visualized radiographically, commonly on the right. DSPT is more subtle in the postpartum or postoperative period and should be suspected in patients with fever despite antibiotic therapy for presumed endometritis or pelvic infection without evidence of abscess who respond to anticoagulation. Imaging plays a role in identifying OVT or alternative causes of fever and has been found to change clinical management in 39% of patients with refractory puerperal fever; however, a negative imaging study does not exclude ST.

Key Anatomic/Physiologic Issues and Imaging Findings/Techniques
Imaging findings include a focal filling defect within a vein, thickening of the vein wall with increased enhancement related to inflammation, and surrounding fluid and fat stranding. ST usually accompanies a primary infection, which may be evident by imaging and is associated with bacteremia, abscesses, and septic emboli. Vessel involvement relates to the site of primary infection. Complications of ST and associated findings in the head and neck, abdomen and pelvis, and extremities as well as catheter related thrombophlebitis will be reviewed.

Conclusion
The radiologist should have a high index of suspicion for ST and may be the first to suggest this diagnosis. Delayed diagnosis can result in increased morbidity and mortality.