A 78-year-old woman presented with sudden-onset lower extremity edema, abdominal pain, and loss of appetite that developed the day after she fell off her bicycle. Computed tomography showed a simple hepatic cyst, 17 cm in diameter, compressing the inferior vena cava (IVC). Her symptoms resolved following laparoscopic deroofing. Notably, the cyst had remained stable at 12 cm 2 and 4 years prior, without any evidence of IVC compression. Although many guidelines for asymptomatic simple hepatic cysts published to date do not recommend treatment or follow-up regardless of size, our experience suggests the importance of monitoring simple hepatic cysts larger than 12 cm.

Leptomeningeal metastasis (LM) is a rare complication of esophageal adenocarcinoma, with reported cases typically presenting with meningitic, encephalopathic, or multifocal neurologic symptoms. We report a 70-year-old man with metastatic esophageal adenocarcinoma with signet-ring cell features who developed subacute, painless, bilateral visual loss with bilateral optic disc edema as the initial manifestation of probable LM. Symptoms arose four months into first-line folinic acid, fluorouracil, and oxaliplatin (FOLFOX) plus pembrolizumab while all measurable extracranial disease was responding and in the absence of headache, meningismus, or other neurologic symptoms. Contrast-enhanced MRI demonstrated bilateral optic nerve sheath enhancement with subtle linear leptomeningeal enhancement over the cerebral convexities and no parenchymal brain metastases. Over the ensuing days, the patient developed urinary incontinence, gait instability, lower-extremity weakness, and cognitive decline. Cerebrospinal fluid analysis showed markedly elevated protein, lymphocytic pleocytosis, normal glucose, and rare atypical cells suspicious for malignancy; flow cytometry and cultures were negative. Although CSF cytology was not definitively diagnostic, the combined clinical presentation, characteristic MRI findings, and supportive CSF abnormalities in the setting of known metastatic malignancy were consistent with probable LM. Whole-brain radiotherapy was initiated but discontinued after one fraction because of rapid neurologic deterioration, and the patient died four weeks after the diagnosis. This case highlights an unusual presentation of probable LM in esophageal adenocarcinoma, with subacute painless bilateral visual loss and optic disc edema preceding other neurologic manifestations despite concurrent extracranial disease response.

To determine whether heel-free compression bandaging is non-inferior to heel-wrapped bandaging for maintaining interface pressure in adults with venous leg ulcers. Randomised, controlled, parallel-group, non-inferiority trial. Adults with open venous leg ulcers (CEAP C6) treated at a French university hospital were randomised to heel-free or heel-wrapped (control) bandaging for 4-6 weeks. The primary outcome was interface pressure 48 h after the final bandage application, analysed in the per-protocol population. Secondary outcomes were ankle oedema, change in interface pressure and patient preference. Of 102 randomised patients, 85 were included in the per-protocol analysis. At V3, mean interface pressure was 30.1 mmHg in the heel-free group and 28.4 mmHg in the control group (difference, 1.7 mmHg; 95% CI, -1.3 to 4.6), meeting the non-inferiority criterion. After adjustment for baseline circumference and sex, ankle circumference was 1.7 cm lower in the heel-free group (95% CI, -3.35 to 0.04). Among 48 patients who had experienced both techniques, 23 (47.9%) preferred heel-free bandaging. Heel-free bandaging was non-inferior to heel-wrapped bandaging for interface pressure at 48 h. The technique may be considered when compatible with ulcer location and patient preference; effects on healing and adherence require further study. Trial Registration: NCT04046120.

Bilateral deep vein thrombosis is rare in adolescents and represents an uncommon presentation of venous thromboembolism.This case describes bilateral deep vein thrombosis in a patient with congenital rubella syndrome and chronic cardiovascular complications.Persistent bilateral lower limb edema in such patients should prompt consideration of deep vein thrombosis.

Lumbosacral transitional vertebrae may alter load transfer and are associated with degenerative changes at spinal levels cranial to the transitional segment. However, the relationship between complete L5 sacralization and pathology at L3-L4 remains uncertain. We report a 69-year-old woman with chronic low-back pain, lower-extremity symptoms, and walking intolerance in the setting of complete bilateral L5 sacralization, L3-L4 grade I anterolisthesis, severe central canal stenosis, and Modic type 1 endplate changes. Given her cardiovascular comorbidity, functional goals, and preference for nonoperative care, she underwent nine months of individualized multimodal conservative management that included low-force pelvic blocking, motorized flexion-distraction therapy, radial shockwave therapy applied to symptomatic soft tissues, home advice, and progressive exercise. At month nine, pain improved from 8/10 to 1/10, lower-extremity symptoms resolved, neural-tension tests were negative, and the patient returned to unrestricted restaurant work. Follow-up magnetic resonance imaging reported L3-L4 anterolisthesis of 0.53 cm compared with 0.65 cm at baseline, together with less apparent marrow edema and facet fluid. This case documents clinical improvement during multimodal conservative care in a patient with complex degenerative lumbar pathology and complete L5 sacralization. The observed imaging differences do not establish true slip reduction, identify the effective treatment component, or confirm a causal biomechanical mechanism. Prospective studies using standardized imaging acquisition, blinded repeated measurements, and comparison groups are required.

Necrotizing myopathy typically presents with subacute symmetric proximal weakness and marked creatine kinase elevation. Acute areflexic paraparesis with sensory abnormalities may instead suggest Guillain-Barré syndrome and create uncertainty regarding neuromuscular localization. A man in his 50s presented after collapse with abrupt bilateral lower-extremity paralysis. Examination demonstrated 0/5 strength across proximal and distal lower-extremity muscle groups, marked rigidity and hypercontracture, areflexia, and sensory impairment, with preserved upper-extremity function. Early laboratory abnormalities included serum sodium 164 mmol/L, potassium peaking at 6.5 mmol/L, creatinine 4.96 mg/dL, blood urea nitrogen 194 mg/dL, creatine kinase greater than 60,000 IU/L, and marked aminotransferase elevations. Lumbar puncture on hospital day (HD) 3 showed cerebrospinal fluid protein 70 mg/dL, glucose 66 mg/dL, and fewer than one nucleated cell/mm3. Guillain-Barré syndrome remained an early consideration; intravenous immunoglobulin was administered, and hemodialysis was initiated for severe hyperkalemia in the setting of acute renal failure. Inpatient electromyography and nerve conduction studies were unavailable; therefore, a concurrent neuropathic process could neither be confirmed nor excluded. Bilateral thigh magnetic resonance imaging demonstrated diffuse intramuscular edema, and right-thigh biopsy subsequently established a necrotizing myopathic pattern with frequent necrotic and regenerating myofibers and sparse inflammation. The biopsy pattern was etiologically nonspecific, and the underlying cause remained unresolved. This case illustrates that areflexia and cerebrospinal fluid albuminocytologic dissociation should not override substantial biochemical, radiographic, and histopathologic evidence of muscle injury. In patients with acute paralysis and massive creatine kinase elevation, neuropathic and myopathic processes should be evaluated in parallel.

Carcinoid heart disease (CHD) is a complication of carcinoid syndrome that results from chronic exposure of the endocardium to circulating vasoactive substances, particularly serotonin. It leads to progressive right-sided valvular dysfunction and right heart failure. Presentation as cardiogenic shock is uncommon and may delay recognition of the underlying disease. We present the case of a 44-year-old woman with no prior medical history who developed progressive dyspnea, ascites, and lower extremity edema over four months and was admitted with cardiogenic shock. Transthoracic echocardiography revealed massive tricuspid regurgitation and moderate-to severe pulmonary regurgitation with marked right ventricular dilation with preserved conventional systolic indices. Abdominal imaging demonstrated hepatomegaly with multiple hypervascular hepatic lesions, and liver biopsy confirmed metastatic neuroendocrine tumor. Urinary 5-hydroxyindoleacetic acid was markedly elevated at 305 mg/24 hours with pro-B-type natriuretic peptide (pro-BNP) at 2,450 pg/mL, supporting the diagnosis of carcinoid syndrome with cardiac involvement. Lanreotide was initiated for biochemical and symptomatic control of the underlying carcinoid syndrome. Despite intensive hemodynamic support with inotropic and vasopressor therapy, the patient developed refractory cardiogenic shock and died from progressive right-sided heart failure. This case highlights an unusual and aggressive presentation of carcinoid disease manifesting as cardiogenic shock. Clinicians should maintain a high index of suspicion for CHD in patients with unexplained right-sided valvular dysfunction and systemic congestion, as early recognition may allow timely therapeutic intervention.

Chronic wounds remain a significant clinical challenge despite advances in dressings, biologics, and adjunctive therapies. Patients referred to advanced wound centers following unsuccessful treatment often demonstrate recurring and potentially correctable factors that contribute to delayed healing. Drawing upon observations from a quaternary referral wound center, this article focuses on recurring and potentially correctable factors encountered during evaluation of wounds that have failed to progress despite prior care. Although these patterns are neither novel nor unexpected, they continue to recur despite well-established wound care principles and treatment guidelines. This article highlights common pitfalls identified in patients referred for advanced wound care evaluation. Commonly encountered issues include inadequate implementation of compression therapy and lower extremity elevation, ineffective offloading in diabetic foot ulcers, limited attention to patient adherence and behavioral factors, and incomplete evaluation of underlying contributors to wound chronicity. Additional patterns include continued use of outdated or nonevidence-based topical agents, misapplication of debridement principles (particularly removal of stable eschar), and incomplete evaluation of underlying pathophysiology such as vascular insufficiency. Patients are frequently referred after undergoing advanced interventions, including hyperbaric oxygen therapy and grafting procedures, before optimization of fundamental wound care principles. In these settings, suboptimal patient selection and sequencing of therapy, particularly in the presence of uncontrolled edema or inadequate offloading, may contribute to prolonged treatment without clinical benefit. These observations highlight recurring gaps between recommended care and real-world execution. Recognition of these recurring pitfalls may improve wound healing outcomes, promote more effective use of advanced therapies, and reduce the need for escalation of care.

We report a 35-year-old man with chronic hepatitis B infection and decompensated liver cirrhosis who presented with an 8-month history of progressive fatigue, exertional limb weakness, anorexia, and dark urine, which partially improved following hepatoprotective and anti-cholestatic therapy. One day before admission, his condition deteriorated abruptly, with fever, chills, diarrhea, profound fatigue, and rapidly progressive bilateral lower-extremity oedema. Laboratory evaluation revealed severe systemic inflammation and coagulopathy, including a white blood cell count of 8.4 × 10[9]/L with neutrophil predominance (absolute neutrophil count, 7.6 × 10[9]/L; neutrophil percentage, 90.7%), severe thrombocytopenia (23 × 10[9]/L), markedly elevated inflammatory markers (C-reactive protein, 68.7 mg/L; procalcitonin, 5.81 ng/mL; interleukin-6, >5000 pg/mL), hypoalbuminemia, and prolonged prothrombin time. Empirical antimicrobial therapy was initiated immediately. Blood cultures obtained on admission became positive within 24 hours and were subsequently identified as Vibrio vulnificus. Antimicrobial therapy was adjusted according to susceptibility testing, and surgical incision, drainage, and debridement were performed for progressive lower-extremity soft tissue infection. The patient gradually improved after pathogen-directed antimicrobial therapy and surgical source control and was discharged after clinical stabilization. This case highlights the importance of early recognition, appropriate antimicrobial therapy, and timely surgical intervention in severe V. vulnificus infection, particularly among patients with underlying liver disease.

Identification of causes for venous outflow obstruction often requires multimodal evaluation. Anchoring bias can challenge recognition of rare pathophysiology, even when common imaging findings are found in uncommon locations. In this review, we present a case of a female patient with several months of right lower extremity edema. Initial misinterpretation of ultrasonography led to the diagnosis of deep vein thrombus as the instigating factor for which the patient was unsuccessfully treated with oral anticoagulation. Cross-sectional imaging and venography were employed showing external compression of the common femoral vein by a cystic structure. Subsequent percutaneous aspiration led to immediate improvement in venous flow by venography. Advanced MR imaging and arthrography were employed showing a labral tear with recurrence of a prominent paralabral cyst compressing the common femoral vein. The patient was managed with definitive arthroscopic cyst decompression and labral repair leading to complete resolution of the patient's presenting symptoms. This case underscores the American College of Radiology (ACR) appropriateness criteria recommending cross-sectional imaging when patients present with inconclusive vascular ultrasound or suspected iliofemoral thrombus. It also adds to well established data that high recurrence rates of paralabral cysts are noted after percutaneous aspiration while lower recurrence is noted with arthroscopic labral repair and cyst decompression.