Faculty Bibliography

OBJECTIVE:Prior authorization (PA) is a process used by payers for safety and cost savings purposes, but it has received criticism for being time-consuming and costly because of administrative burden. Our study evaluated efficacy of PA applied to in-office lower extremity superficial venous procedures. METHODS:All in-office lower extremity venous procedures scheduled to be performed at our institution in 2017 were included in the study. Variables of interest were type of procedure, initial PA status (approved or denied), rationale for the decision, and final status after appeal. Cost analysis was performed using Centers for Medicare and Medicaid Services allowable rates to approximate billing and reimbursement data (proprietary) as well as calculated using industry averages. RESULTS:For 2017, of 1959 procedures scheduled, 57.9% (n = 1134) required PA. Of these, only 6.1% (n = 69) received initial PA denial, and nearly 40% of the denials (n = 27) were overturned after appeal. Of the 42 denials that were upheld, 15 resulted in cancellations; the remainder were performed by patient self-pay (n = 11) or by the provider pro bono (n = 16). Overturned denials were a result of either submission of incomplete clinical data on initial PA request or insufficient documentation of clinical necessity. When Centers for Medicare and Medicaid Services allowable rates were applied for cost analysis, the denials resulted in <$60,000 payer savings. Administrative expenses totaled >$110,000 when industry standards were applied, which far exceeds any calculated payer savings using the same methods. The 15 denials resulting in procedure cancellations (1.3% of all PAs) could be considered a net savings to the health care system but only approximated a mere $30,000. CONCLUSIONS:Our study demonstrates that PA is not a cost-effective measure for utilization management of outpatient superficial venous procedures when surgeon practices are already well aligned with insurance guidelines. For these physicians and physician groups, the administrative cost associated with the PA process exceeds the savings seen by the insurance companies.

OBJECTIVE:MATERIAL AND METHODS: This is a single tertiary care center retrospective cohort study of all consecutive inpatients diagnosed with acute VTE from June 2015 to December 2015. During this period, 4495 patients underwent venous duplex examination (622 UE and 3873 LE), identifying 83 inpatient DVTs. Chronic DVT as well as those diagnosed in the outpatient population were excluded. DVTs were classified as either provoked or unprovoked. Provoked DVT were defined as the presence of any of the following factors within 30 days prior to diagnosis: major surgery, immobilization (greater than 3 days of bedrest), trauma, infection requiring antibiotics, central venous access, pregnancy, and/or hormonal medication use. Inpatient pulmonary embolisms (PE) detected on chest computed tomography (CT) were also evaluated during this time frame. Patient data were collected including age, gender, race, lifestyle factors, comorbidities, VTE risk factors, symptomatology at presentation, management including anticoagulation choice and filter placement if applicable, as well as discharge disposition. Statistical analysis was performed using GraphPad Prism 8.0 (GraphPad Software, San Diego, California, USA), and a threshold p-value of < 0.05 set for significance. RESULTS:During the study period, 83 DVTs (48 LEDVT, 35 UEDVT) and 24 PE were identified in 96 inpatients. Of these DVTs, 77.1% of these were defined as provoked. Eleven patients had simultaneous DVT and PE, and thirteen patients had PE with presumed occult pelvic or LEDVT. UEDVT patients had a higher proportion of comorbidities than LEDVT patients: coronary artery disease (25.7% vs. 13.1%, p=0.16), congestive heart failure (20% vs. 6.6%, p=0.09), as well as a trend toward higher incidence of malignancy (60% vs. 42.6%, p=0.13). Of provoked VTE, UEDVT correlated more significantly with central venous catheters (88.4% vs. 12.5%, p=<0.0001), but was less commonly associated with prolonged bed rest (19.2% vs. 39.5%, p=0.11). PE was diagnosed in 24/96 (25%) of the study population. Patients with LEDVT were found to have a significantly higher incidence of PE compared to those with UEDVT (34.4% vs. 8.6%, p=0.006). Same-admission mortality for patients with VTE was 13/96 (13.5%). Of these, patients with UEDVT had significantly higher all-cause mortality than patients with LEDVT (28.5% vs. 4.9%, p=0.004). When catheter-related UEDVT were excluded, there remained a significant difference in mortality between non-catheter related UEDVT and LEDVT (33.3% vs. 4.9% p=0.0119). CONCLUSIONS:This study demonstrates a high prevalence of UEDVT in hospitalized patients who experience VTE. Despite a lower incidence of synchronous PE, patients with UEDVT had a higher prevalence of significant medical comorbidities and higher all-cause mortality on the index hospital admission.

Objective: Abdominal aortic aneurysm (AAA) is a fatal vascular disease on rupture with still limited mechanistic knowledge of the pathophysiologic process. We sought to determine the heterogeneous cell subtypes and to characterize the spectrum of transcriptome signatures in each cell population within the aneurysmal wall by unbiased single-cell RNA sequencing (scRNA-seq) of human AAA tissue.
Method(s): Aortic specimens were collected from AAA and control healthy organ donor. Samples were processed by enzymatic digestion and mechanical disruption to generate single-cell suspension. Single-cell RNA libraries were prepared after generation of single-cell beads in emulsion. Sequencing was performed on a NovaSeq 6000 platform (Illumina, San Diego, Calif). After alignment, barcode assignment, and sample de-multiplexing, data analysis was performed on t-distributed stochastic neighbor embedding charts of cell transcriptome. Cell clusters were identified by unsupervised proximity based on Euclidian distance and supervised identification of biologic markers within clusters. Pathway analysis algorithms were used to outline biologically relevant networks.
Result(s): Unbiased analysis of scRNA-seq data sets showed 19 different cell clusters with unique transcriptomic signatures in AAA. A total of 8826 significant differentially expressed genes were identified in AAA vs control. Notably, gene transcription-associated extracellular matrix remodeling (COL1A1, COL3A1, COL1A2, LUM), Wnt signaling modulation (SFRP2), and synthetic cellular phenotypes (RPS29, RPS27, RPL13A, RPL28) were among the top increased profiles in AAA tissue. Pathway enrichment analysis of AAA vs control libraries revealed significant modulation of cell proliferation, cell-extracellular matrix interaction, neoangiogenesis, and inflammation. Five novel cell clusters with distinct immune synthetic phenotypes were predominantly abundant in AAA wall compared with the healthy aorta. A robust enrichment in immune cell entities was identified in AAA but not in control tissues, including expansion of CD19⁺ B lymphocytes and a subset of CD3E⁺ T lymphocytes significantly expressing IL32 and CCL5. In contrast, smooth muscle cell (ACTA2⁺MYH11⁺) number declined in AAA but revealed increased transcription of the protease ADAMTS4 and inflammatory signals (CCL19, CCL21, IL6, CCL2). Intercluster pathway analysis revealed enrichment of eukaryotic initiation factor 2 and mechanistic target of rapamycin signaling in the AAA macrophage population along with an increased number of inflammatory and T-cell activation cascades.
Conclusion(s): To the best of our knowledge, this is the first report of scRNA-seq analysis on human AAA. This cutting-edge technique uncovered novel cell clusters and provided a comprehensive understanding of cellular spatiotemporal changes within the AAA wall. Here we provide novel interconnected mechanistic insights into this complex disease to enrich our understanding of AAA development.
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Guideline 1.1: Compression after thermal ablation or stripping of the saphenous veins. When possible, we suggest compression (elastic stockings or wraps) should be used after surgical or thermal procedures to eliminate varicose veins. [GRADE - 2; LEVEL OF EVIDENCE - C] Guideline 1.2: Dose of compression after thermal ablation or stripping of the varicose veins. If compression dressings are to be used postprocedurally in patients undergoing ablation or surgical procedures on the saphenous veins, those providing pressures >20 mm Hg together with eccentric pads placed directly over the vein ablated or operated on provide the greatest reduction in postoperative pain.[GRADE - 2; LEVEL OF EVIDENCE - B] Guideline 2.1: Duration of compression therapy after thermal ablation or stripping of the saphenous veins. In the absence of convincing evidence, we recommend best clinical judgment to determine the duration of compression therapy after treatment. [BEST PRACTICE] Guideline 3.1: Compression therapy after sclerotherapy. We suggest compression therapy immediately after treatment of superficial veins with sclerotherapy to improve outcomes of sclerotherapy. [GRADE - 2; LEVEL OF EVIDENCE - C] Guideline 3.2: Duration of compression therapy after sclerotherapy. In the absence of convincing evidence, we recommend best clinical judgment to determine the duration of compression therapy after sclerotherapy. [BEST PRACTICE] Guideline 4.1: Compression after superficial vein treatment in patients with a venous leg ulcer. In a patient with a venous leg ulcer, we recommend compression therapy over no compression therapy to increase venous leg ulcer healing rate and to decrease the risk of ulcer recurrence. [GRADE - 1; LEVEL OF EVIDENCE - B] Guideline 4.2: Compression after superficial vein treatment in patients with a mixed arterial and venous leg ulcer. In a patient with a venous leg ulcer and underlying arterial disease, we suggest limiting the use of compression to patients with ankle-brachial index exceeding 0.5 or if absolute ankle pressure is >60 mm Hg. [GRADE - 2; LEVEL OF EVIDENCE - C].