Persistent opioid use after curative-intent hepatectomy for neoplastic disease.

BACKGROUND AND OBJECTIVES: This study analyzed persistent opioid use in opioid-naïve and nonopioid-naïve patients undergoing hepatectomy for neoplastic disease. METHODS: A retrospective review was performed of a prospective database using inclusion criteria of hepatectomy for neoplastic disease from October 2013 to December 2017. Prescription data were collected from the North Carolina Controlled Substance Reporting System. Persistent opioid use was defined as patients who continued filling opioid prescriptions 90 days to 1 year after surgery. Patients who did not receive opioid prescriptions between 12 months and 31 days before surgery were defined as naïve. RESULTS: The analysis included 75 surgeries on naïve and 58 surgeries on nonnaïve patients. 56% of naïve patients and 79% of nonnaïve patients developed persistent opioid use, respectively (p = .0056). Naïve patients received 2.24 ± 4.30 MMEs/day, while nonnaïve patients received 5.50 ± 5.98 MMEs/day during Postoperative days 90-360 (95% CI, 1.41-5.10; p < .001). Naïve patients with a lower Preoperative ECOG score were more likely to develop persistent opioid use (OR, 0.45; 95% CI, 0.21-0.99; p = .048). CONCLUSION: More than half of naïve patients undergoing hepatectomy developed persistent opioid use within the first year, though significantly less than nonnaïve patients. Improved performance status was associated with an increased risk of persistent opioid use in naïve patients.

20th SFG(A) Non-Trauma Module (NTM) Course.

The authors describe the 20th Special Forces Group-Airborne Non-Trauma Module refresher training for Special Forces medical sergeants and Special Operations combat medics.

Pleiotrophin produced by multiple myeloma induces transdifferentiation of monocytes into vascular endothelial cells: a novel mechanism of tumor-induced vasculogenesis.

Enhanced angiogenesis is a hallmark of cancer. Pleiotrophin (PTN) is an angiogenic factor that is produced by many different human cancers and stimulates tumor blood vessel formation when it is expressed in malignant cancer cells. Recent studies show that monocytes may give rise to vascular endothelium. In these studies, we show that PTN combined with macrophage colony-stimulating factor (M-CSF) induces expression of vascular endothelial cell (VEC) genes and proteins in human monocyte cell lines and monocytes from human peripheral blood (PB). Monocytes induce VEC gene expression and develop tube-like structures when they are exposed to serum or cultured with bone marrow (BM) from patients with multiple myeloma (MM) that express PTN, effects specifically blocked with antiPTN antibodies. When coinjected with human MM cells into severe combined immunodeficient (SCID) mice, green fluorescent protein (GFP)-marked human monocytes were found incorporated into tumor blood vessels and expressed human VEC protein markers and genes that were blocked by anti-PTN antibody. Our results suggest that vasculogenesis in human MM may develop from tumoral production of PTN, which orchestrates the transdifferentiation of monocytes into VECs.

Intravascular B-cell lymphoma: case report of a rare cause of pulmonary arterial hypertension.

BACKGROUND: Intravascular large B-cell lymphoma (IVLBCL) is a rare disease characterized by proliferation of malignant lymphoid cells within the small vessels of various organs resulting in diffuse thrombosis. It most commonly affects the central nervous system and the skin, but if it involves the pulmonary arteries it can cause acute severe pulmonary hypertension (PH) and right heart failure. Early diagnosis is essential as the clinical course is extremely aggressive. In this report, we present a case of rapidly progressive PH and subsequent right ventricular (RV) failure secondary to IVLBCL. We review the important differential diagnoses and diagnostic evaluation needed to make a correct and early diagnosis. CASE SUMMARY: A 53-year-old, previously healthy man developed 2 months of progressive shortness of breath. After being treated for presumptive pneumonia, he was admitted with hypoxic respiratory failure, altered mental status, and severe PH. He developed RV failure and subsequent liver failure. He was ruled out for pulmonary embolism. Despite aggressive management with inhaled nitric oxide and epoprostenol, inotropes, and continuous renal replacement therapy, the patient passed away. Post-mortem examination revealed the presence of IVLBCL with extensive involvement notable of the brain, heart, lungs, and pulmonary arteries. DISCUSSION: The acute development of severe PH and RV failure in the absence of pulmonary emboli is uncommon and represents a challenging diagnostic and management clinical scenario. When accompanied by altered mental status, constitutional symptoms and an elevated lactate dehydrogenase, clinicians should have a high index of suspicion for intravascular lymphoma, as early diagnosis is critical to maintain a reasonable chance of survival.

Long-term clinical outcomes of focal impulse and rotor modulation for treatment of atrial fibrillation: A multicenter experience.

BACKGROUND: New approaches to ablation of atrial fibrillation (AF) include focal impulse and rotor modulation (FIRM). Studies of this technology with short-term follow-up have shown favorable outcomes. OBJECTIVE: The purpose of this study was to characterize the long-term results of FIRM ablation in a cohort of patients treated at 2 academic medical centers. METHODS: All FIRM-guided ablation procedures (n = 43) at UCLA Medical Center and Virginia Commonwealth University Medical Center performed between January 2012 and October 2013 were included for analysis. During AF, FIRM software constructed phase maps from unipolar atrial electrograms to identify putative AF sources. These sites were targeted for ablation, along with pulmonary vein isolation in 77% of patients. RESULTS: AF was paroxysmal in 56%, and 67% had prior AF ablation. All patients had rotors identified (mean 2.6 ± 1.2 per patient, 77% in LA). Prespecified acute procedural end-point was achieved in 47% of patients (n = 20): AF termination in 4, organization in 7, >10% slowing of AF cycle length in 9. Acute complications occurred in 4 patients (9.3%). At 18 ± 7 months of follow-up, 37% were free from documented recurrent AF after a 3-month blanking period; 21% were free from documented atrial tachyarrhythmias and off antiarrhythmic drugs. Multivariate analysis did not reveal any significant predictors of AF recurrence, including pattern of AF, acute procedural success, or prior failed ablation. CONCLUSION: Long-term clinical results after FIRM ablation in this cohort of patients showed poor efficacy, different from previously published studies. Randomized studies are needed to evaluate the efficacy and clinical utility of this ablation approach for treating AF.

Quantitative analysis of localized sources identified by focal impulse and rotor modulation mapping in atrial fibrillation.

BACKGROUND: New approaches to ablation of atrial fibrillation (AF) include focal impulse and rotor modulation (FIRM) mapping, and initial results reported with this technique have been favorable. We sought to independently evaluate the approach by analyzing quantitative characteristics of atrial electrograms used to identify rotors and describe acute procedural outcomes of FIRM-guided ablation. METHODS AND RESULTS: All FIRM-guided ablation procedures (n=24; 50% paroxysmal) at University of California, Los Angeles Medical Center were included for analysis. During AF, unipolar atrial electrograms collected from a 64-pole basket catheter were used to construct phase maps and identify putative AF sources. These sites were targeted for ablation, in conjunction with pulmonary vein isolation in most patients (n=19; 79%). All patients had rotors identified (mean, 2.3±0.9 per patient; 72% in left atrium). Prespecified acute procedural end point was achieved in 12 of 24 (50%) patients: AF termination (n=1), organization (n=3), or >10% slowing of AF cycle length (n=8). Basket electrodes were within 1 cm of 54% of left atrial surface area, and a mean of 31 electrodes per patient showed interpretable atrial electrograms. Offline analysis revealed no differences between rotor and distant sites in dominant frequency or Shannon entropy. Electroanatomic mapping showed no rotational activation at FIRM-identified rotor sites in 23 of 24 patients (96%). CONCLUSIONS: FIRM-identified rotor sites did not exhibit quantitative atrial electrogram characteristics expected from rotors and did not differ quantitatively from surrounding tissue. Catheter ablation at these sites, in conjunction with pulmonary vein isolation, resulted in AF termination or organization in a minority of patients (4/24; 17%). Further validation of this approach is necessary.