A 66-year-old Caucasian female presented with persistent fever (38.7 degrees Celsius) and non-productive cough with onset 4 weeks prior, and despite 2 courses of antibiotics, she developed right-sided neck swelling and pain about 2 weeks prior to admission. Significant medical history included Immunoglobulin G (IgG) deficiency that was diagnosed nine months prior, and for the last three months, she received monthly injections via an implanted right chest port without complications.
She was febrile (38.3 degrees Celsius), tachycardic (119 bpm), and hypertensive (191/110 mm/Hg) on admission. There was significant edema and tenderness to palpation at the right neck near the mid-sternocleidomastoid muscle, which extended to the right mandibular angle. Leukocyte count was 12.4 x103/µL with 80% neutrophils. Computerized tomography (CT) of the neck with contrast demonstrated right internal jugular vein (IJV) thrombophlebitis and subcutaneous edema and emphysema surrounding the right chest port and along the right pectoralis muscle.
Diagnosed with sepsis secondary to right IJV thrombophlebitis associated with chest port, she received intravenous (IV) fluids and antibiotics. Chest port was accessed, but non-functional. On hospital day 2, chest port was removed, and there were no signs of infection of the port or at the implantation site. On hospital day 3, fever and leukocytosis worsened despite negative blood, port, and catheter tip cultures, and oral anti-coagulation was started. Repeat CT neck showed unchanged right IJV thrombophlebitis, but noted a right upper lobe consolidation. Non-contrasted CT chest showed multifocal air space opacities and granulomatous disease. By hospital day 4, fever and leukocytosis resolved, and neck swelling and pain began to improve. On hospital day 7, she underwent bronchoalveolar lavage (BAL) because prior BAL reported Actinomyces odontolyticus. On hospital day 8, she was discharged on oral antibiotics and anticoagulation. BAL resulted Actinomyces graevenitzii 3 days after discharge.
Discussion:
Jugular vein thrombophlebitis can be caused by endothelial trauma from intravenous catheters. This patient’s physical exam and CT imaging were consistent with this diagnosis. Initial cultures were negative, and it is possible that her antimicrobial therapies prior to admission may have affected these results. Her persistent bronchitis and fever could have raised suspicion for Lemierre’s Syndrome. Lemierre’s syndrome is characterized by an initial pharyngitis, commonly caused by Fusobacterium necrophorum, that evolves into suppurative jugular vein thrombophlebitis. This is caused by extension of the infection from the peritonsillar space to the jugular vein via the lateral pharyngeal area. Repeat imaging on this patient revealed a new pneumonia, which can also be a secondary manifestation of Lemierre’s Syndrome. Inconsistent with Lemierre’s Syndrome, however, was the causative organism of her upper respiratory infection, Actinomyces graevenitzii. It may be deduced that this patient’s immunocompromised state secondary to IgG deficiency increased her risk of infections by uncommon pathogens.
Conclusions:
Internal jugular vein thrombophlebitis can be caused by intravenous catheters, but if it is preceded by pharyngitis or an URI with persistent fever, Lemierre’s Syndrome should be of high clinical suspicion. If there is a concomitant immunocompromised state, uncommon pathogens should be considered for the causative organism.