Head, Neck, and Abdominopelvic Septic Thrombophlebitis: Current Evidence and Challenges in Diagnosis and Treatment

Abstract

Septic thrombophlebitis (STP) is a complex, cross-disciplinary clinical condition that combines a localized infection with a neighboring venous thrombosis. STP can occur at several possible anatomic sites, such as dural sinuses, jugular vein (Lemierre syndrome), portal vein (pylephlebitis), and pelvic veins. Its high mortality in the preantibiotic era improved considerably with the introduction of modern antibiotics. However, little evidence exists to date to guide its clinical management. The incidence of STP or its risk factors may be increasing, and its mortality may still be considerable. These trends would have far-reaching implications, especially in the setting of increasing resistance to antimicrobial agents. No clinical assessment tools exist to support patient screening or guide treatment in STP. Few interventional studies exist on the efficacy and safety of anticoagulation. Recommendations on its indications, duration, and the agents of choice are mostly based on evidence derived from small observational studies. While all forms of STP pose similar challenges, future research may benefit from the distinction between bacteria-associated, virus-associated, and mycosis-associated thrombophlebitis. Addressing these gaps in evidence would enhance our ability to diagnose this condition and treat patients effectively.

Lupus anticoagulant hypoprothrombinemia syndrome associated with bilateral adrenal haemorrhage in a child: early diagnosis and intervention

“…Antibodies promoting thrombosis are known to be associated with autoimmune diseases, such as antiphospholipid syndrome, or to be produced in reaction to an acute infection, particularly in children [13,14]. However, our patient developed SLE after 1 year, a development described less frequently than the opposite one [9,15].…”

Venous Thromboembolic Disease in Chronic Inflammatory Lung Diseases: Knowns and Unknowns

“…Specifically, it was reported that the adjusted odds ratio (OR) was 1.4 (95% CI 1.4–1.5) for PE, 1.6 (95% CI 1.5–1.7) for DVT, and 1.6 (95% CI 1.3–2.0) for both entities in asthma patients compared to healthy individuals ( Table 1 ). Earlier, a nationwide cohort study by Chung et al [ 9 ] showed that the overall incidence rate of PE was three times higher in 31,356 patients with newly diagnosed asthma compared to 125,157 non-asthmatic individuals (10.2 versus 3.1 per 100,000 person-years). The overall hazard ratio (HR) of PE in asthmatic patients was 3.2 (95% CI 1.7–6.0), after adjusting for sex, age, comorbidities, and estrogen use ( Table 1 ).…”

“…An unambiguous relationship between the frequency of emergency department visits because of asthma exacerbations and PE incidence has been stated [ 24 ]. Chung et al supported that the adjusted HR for PE increased from 1.0 (95% CI 0.3–2.9) for those having two or fewer visits to 9.0 (95% 4.3–18.9) for those with four or more visits [ 9 ]. Similarly, Zöller et al found that the OR for PE shaping from 1.3 (95% CI 1.3–1.4) for one to two hospital admissions to 1.4 (95% CI 1.3–1.6) for three or four admissions and 1.82 for more than four hospital admissions [ 24 ].…”

“…NETs can activate factor (F) VII and TF, bind to von Willebrand factor (vWF), activate platelets via H3 and H4 histones, and locally concentrate enzymes such as neutrophil elastase and myeloperoxidase which cleave and inactivate TF pathway inhibitor (TFPI) and thrombomodulin [ 6 ], triggering immunothrombosis. Moreover, through largely overlapping pathways, and with the possible additional mediation of agent-specific virulence factors or autoantibodies, infection by both viruses [ 8 ] and bacteria [ 9 ], to which patients with chronic and acute respiratory disease are particularly vulnerable, has been postulated to cause local or systemic thrombophlebitis.…”

Sex differences in Lemierre syndrome: Individual patient-level analysis

“…Little is known of the epidemiology and clinical course of LS, and sex differences have never been investigated so far. Yet, the pathophysiology of LS may involve an interplay of the coagulation cascade with components of innate and adaptive immunity [2] known to display sex differences [3], particularly in bacterial sepsis [4] and in the age groups most affected by LS [5]. Since the condition has a prominent thrombotic component, the known sex differences in non-septic venous thromboembolism may also apply to it.…”