Objectives Chronic refractory lower-extremity edema often remains undiagnosed despite standard evaluations that focus primarily on excluding deep vein thrombosis. We aimed to elucidate the underlying etiologies and assess the utility of a comprehensive, structured diagnostic protocol. Methods We retrospectively analyzed a prospectively enrolled, referral-based cohort of 58 patients with chronic refractory lower- extremity edema who underwent a structured multimodal diagnostic protocol after failure of standard noninvasive evaluation. Etiologies were classified as non-thrombotic iliac vein lesions, pulmonary hypertension, superficial venous insufficiency, or multifactorial. Results Non-thrombotic iliac vein lesions, pulmonary hypertension, and superficial venous insufficiency were identified in 55.2%, 48.3%, and 43.1% of patients, respectively. Single etiologies accounted for 51.7% of cases, 41.4% were multifactorial, and 6.9% remained unclassified. Among pulmonary hypertension cases, isolated postcapillary pulmonary hypertension associated with heart failure with preserved ejection fraction was the most common (13.8%). Superficial venous insufficiency was the sole cause in 12.1% of cases, while in others, it coexisted with non-thrombotic iliac vein lesions or pulmonary hypertension. Interventions included iliocaval endovascular therapy (n = 23) and saphenous vein ablation ( n = 10), with the remainder receiving conservative therapy. Over a median follow-up of 2.98 years, 86.2% of patients achieved objective clinical improvement. Conclusions This protocol reduced the number of repeated low-yield ultrasound examinations and facilitated targeted treatment. A structured diagnostic protocol integrating duplex ultrasonography, invasive hemodynamic testing, and intravascular imaging enables accurate etiologic classification of chronic refractory lower extremity edema. This approach identifies treatable contributors, supports tailored interventions, and may improve outcomes while reducing unnecessary testing.
Background Hyperkalemia is a common and potentially life-threatening electrolyte disorder often associated with chronic kidney disease (CKD) and heart failure (HF). Despite available guidance for acute management, outpatient approaches remain variable across specialties, often resulting in inconsistent treatment and premature discontinuation of guideline-directed medical therapies (GDMTs). A multidisciplinary, consensus-based outpatient hyperkalemia care pathway that integrates identification, risk classification, treatment, and monitoring recommendations across primary care, cardiology, and nephrology care settings was developed to standardize care for patients with hyperkalemia. Methods Two roundtable sessions were conducted to identify key barriers to outpatient hyperkalemia management and subsequently develop the consensus Multidisciplinary Outpatient Hyperkalemia Care Pathway, informed by clinical guidelines. Feedback and perspectives from expert multidisciplinary roundtable clinicians were integrated through iterative rounds of review; the care pathway was further validated via discussion with a primary care physician. Results The consensus-driven Multidisciplinary Outpatient Hyperkalemia Care Pathway outlines a stepwise framework consisting of: (A) a comprehensive assessment and patient work-up, (B) risk classification, (C) individualized dietary and therapeutic management, (D) last-resort GDMT down-titration or discontinuation considerations, (E) GDMT reintroduction recommendations, and (F) long-term monitoring suggestions that integrate referral guidance. Conclusions The Multidisciplinary Outpatient Hyperkalemia Care Pathway provides a structured approach designed to reduce hyperkalemia care variability and support coordinated multidisciplinary care when implemented in clinical practice. Trial Registration Not applicable.
Abstract Introduction Blastomycosis, caused by Blastomyces dermatitidis, is a dimorphic fungus endemic to the Ohio and Mississippi River valleys. The fungus primarily affects the lungs following inhalation of conidia, which evade immune clearance and convert to yeast, inciting granulomatous inflammation (1). Pulmonary blastomycosis often mimics bacterial pneumonia, tuberculosis, or malignancy, complicating timely diagnosis. Radiographic findings are variable, with airspace consolidation being most common; cavitary lesions are rare. Diagnosis becomes particularly challenging in patients with coal workers’ pneumoconiosis, especially in its severe form—progressive massive fibrosis (PMF)—which features large fibrotic masses that may cavitate. Case Presentation A 67-year-old male with a history of OSA, COPD, hypertension, and pneumoconiosis with PMF presented to the pulmonology clinic with chronic exertional dyspnea, cough with thick clear sputum, and paroxysmal nocturnal dyspnea. He denied orthopnea, fever, night sweats, or hemoptysis. Chest CT revealed mass-like opacifications and scattered nodules consistent with PMF, along with an irregular cavitary consolidation in the posterior right infra hilar region extending to the superior segment of the right lower lobe. Bronchoscopy was performed, and fungal cultures from bronchial washings grew Blastomyces dermatitidis. The patient was started on oral itraconazole. Discussion This case underscores the diagnostic complexity of pulmonary blastomycosis in the setting of PMF. The patient’s known occupational lung disease and chronic symptoms initially suggested progression of PMF. However, the emergence of cavitary lesions raised concern for superimposed infection. Radiographic manifestations of blastomycosis are diverse, ranging from airspace and lobar consolidation to diffuse interstitial changes (2). Cavitary lesions, though uncommon, should prompt consideration of fungal etiologies, especially in endemic areas. The overlap in imaging findings between PMF and fungal infections can obscure diagnosis, delaying appropriate treatment. Conclusion Blastomycosis should remain a differential consideration in patients with occupational lung disease presenting with new cavitary lesions, particularly in endemic regions. Early recognition and antifungal therapy, typically with itraconazole, are essential to prevent complications. Amphotericin B may be reserved for severe or disseminated disease. This case highlights the importance of maintaining a broad differential and utilizing bronchoscopy and fungal cultures for definitive diagnosis. Reference: 1. Maini R, Ranjha S, Tandan N, et al. Pulmonary blastomycosis: a case series and review of unique radiological findings. Med Mycol Case Rep. 2020;28:49-54. doi:10.1016/j.mmcr.2020.03.006.2. Fang W, Washington L, Kumar N. Imaging manifestations of blastomycosis: a pulmonary infection with potential dissemination. Radiographics. 2007;27(3):641-655. doi:10.1148/rg.273065122. This abstract is funded by: none
