Predictors of endobronchial forceps utilization for inferior vena cava filter retrieval: when snare retrieval fails.

BACKGROUND: Endobronchial forceps are commonly used for complex IVC filter removal and after initial attempts at IVC filter retrieval with a snare have failed. Currently, there are no clear guidelines to help distinguish cases where primary removal should be attempted with standard snare technique or whether attempts at removal should directly be started with forceps. This study is aimed to identify clinical and imaging predictors of snare failure which necessitate conversion to endobronchial forceps. METHODS: Retrospective analysis of 543 patients who underwent IVC filter retrievals were performed at three large quaternary care centers from Jan 2015 to Jan 2022. Patient demographics and IVC filter characteristics on cross-sectional images (degree of tilt, hook embedment, and strut penetration, etc.) were reviewed. Binary multivariate logistic regression was used to identify predictors of IVC filter retrieval where snare retrieval would fail. RESULTS: Thirty seven percent of the patients (n = 203) necessitated utilization of endobronchial forceps. IVC filter hook embedment (OR:4.55; 95%CI: 1.74-11.87; p = 0.002) and strut penetration (OR: 56.46; 95% CI 20.2-157.7; p = 0.001) were predictors of snare failure. In contrast, total dwell time, BMI, and degree of filter tilt were not associated with snare failure. Intraprocedural conversion from snare to endobronchial forceps was significantly associated with increased contrast volume, radiation dose, and total procedure times (p < 0.05). CONCLUSION: IVC filter hook embedment and strut penetration were predictors of snare retrieval failure. Intraprocedural conversion from snare to endobronchial forceps increased contrast volume, radiation dose, and total procedure time. When either hook embedment or strut penetration is present on pre-procedural cross-sectional images, IVC filter retrieval should be initiated using endobronchial forceps. LEVEL OF EVIDENCE: Level 3, large multicenter retrospective cohort.

Endovascular treatment of postpartum haemorrhage in a woman with genitourinary and vascular congenital malformations.

A 43-year-old woman presented with postpartum haemorrhage necessitating uterine artery embolisation. Prior to embolisation, angiography demonstrated the presence of a persistent sciatic artery (PSA). Due to the possibility of embolic particles inadvertently traveling to the lower extremity via this variant arterial pathway, care was taken to only embolise the uterine artery. PSAs are uncommon but important vascular pathways to screen for during pelvic intervention and are associated with other genitourinary anomalies.

Upregulation of HLA-E by dengue and not Zika viruses.

INTRODUCTION: The most severe form of dengue virus (DENV) illness, dengue haemorrhagic fever, is characterised by plasma leakage and increased vascular permeability. OBJECTIVES: Given the critical role that endothelial cells play in the pathogenesis of DENV, we wanted to determine whether infection with DENV altered the expression of MHC class I related genes including HLA-E. RESULTS: In this study, we provide evidence that HLA-E but not MICA/B or HLA-G is upregulated by all four serotypes of DENV in an endothelial cell line human microvascular endothelial cells (HMEC)-1. In contrast, Zika virus (ZIKV), a related flavivirus, where plasma leakage is not a major manifestation of disease, did not upregulate HLA-E. We found modest levels of soluble HLA-E in supernatants from DENV but not ZIKV-infected cells. Coculture experiments found minimal activation of natural killer (NK) cells in the presence of both uninfected and infected HMEC-1 cells. HLA-E induced by DENV infection could not dampen the degranulation of activated NK cells by interacting with its ligand NKG2a. CONCLUSIONS: Our results suggest that while DENV infection induces HLA-E, the high MHC class I expression on uninfected and infected HMEC-1 cells may dominate the diverse signals generated between inhibitory and activating receptors on NK cells and ligands on target cells.