Venous thromboembolism (VTE), comprising deep venous thrombosis (DVT) and pulmonary embolism (PE), are frequently observed during pregnancy and may cause maternal death. During pregnancy, several physiological and anatomical changes occur that enhance thrombotic risk. In addition, this risk might be significantly increased by several patient-specific risk factors. Therefore, VTE risk assessment in all pregnant women is essential for early identification of those at increased risk so as to obtain a timely diagnosis and plan a correct therapeutic approach. Unfortunately, clinical examinations may be complicated by the overlap between common physiological symptoms of pregnancy and those indicative of VTE. Thus, validated clinical decision tools such as the LEFt (Left lower extremity (L), Edema (E) and, symptom onset during the First Trimester of pregnancy) rule for suspected DVT and the YEARS algorithm for suspected PE have been developed to aid diagnostic assessment. Definitive diagnosis of DVT or PE requires confirmation with appropriate imaging modalities. An early diagnosis is important to facilitate prompt initiation of therapy that has Low Molecular Weight Heparin as the cornerstone of prevention and treatment during pregnancy and the postpartum period. In this narrative review, we consider the major risk factors for VTE during pregnancy, key diagnostic algorithms and updated therapeutic approaches.

Waldenström macroglobulinemia (WM) is a rare CD20-positive B-cell non-Hodgkin lymphoma. It is characterized by lymphoplasmacytic infiltration in the bone marrow and abnormal monoclonal IgM secretion. WM complicated by renal amyloidosis is uncommon but associated with rapid progression of organ damage. Accurate identification of pathogenic factors and individualized treatments are essential to improve prognosis. This paper reports the case of a 75-year-old female who initially presented with facial edema and bilateral lower-extremity edema lasting 2 days. Additional symptoms included foamy urine, frequent urination, and urgency. Laboratory tests revealed significant proteinuria (24-h urinary protein, 6.11 g), hypoalbuminemia (serum albumin, 20.07 g/L), and impaired renal function (serum creatinine, 129.90 μmol/L; eGFR, 45.2 mL/min/1.73 m2). Immunofixation electrophoresis detected monoclonal IgM-λ immunoglobulin in both serum and urine. Bone marrow biopsy demonstrated clonal lymphoplasmacytic infiltration (32%), and genetic testing revealed a positive MYD88-L265P mutation (mutation frequency, 28.5%). Renal biopsy indicated diffuse deposition of λ light chains predominantly in the glomerular mesangium. Ultrastructural examination revealed amyloid fibrils, confirming the diagnosis of AL λ - type amyloid nephropathy. Chemotherapy with rituximab, cyclophosphamide, and dexamethasone (RCD regimen), combined with symptomatic supportive therapy, resulted in temporary improvement of clinical symptoms and laboratory parameters. However, the disease progressed rapidly. The patient died on Jan 28, 2024, approximately 3 months after discharge, due to multiple organ failure involving cardiac, renal, and respiratory dysfunction. Based on relevant literature and the Chinese Expert Consensus on Diagnosis and Treatment of Lymphoplasmacytic Lymphoma (LPL)/WM (2022 Edition) [Abstract 3], this paper discusses diagnostic criteria, differentiation of pathogenic components, treatment strategies, and prognostic factors. These findings may provide clinical guidance for similar rare cases.

IntroductionFemoral vein adventitial cystic disease is an exceedingly rare vascular disorder characterized by mucin-filled cysts within the venous wall, leading to potential luminal obstruction and clinical symptoms. This case highlights the diagnostic challenges and management of this uncommon condition.Case PresentationA 58-year-old male presented with a 2-month history of progressive left lower extremity swelling and discomfort. Physical examination revealed pitting edema along the calf. Duplex ultrasound demonstrated a hypoechoic cystic lesion compressing the femoral vein. Contrast-enhanced computed tomography (CT) and magnetic resonance imaging (MRI) confirmed a 3.1 cm × 1.4 cm × 2.1 cm cystic mass within the adventitial layer of the femoral vein, with partial luminal stenosis. No evidence of deep vein thrombosis or malignancy was observed.Intervention and OutcomeSurgical exploration via groin incision identified a translucent cyst arising from the femoral vein adventitia. Complete excision was performed with venous reconstruction. Histopathology confirmed a benign adventitial cyst with mucinous content and a single-layer endothelial lining. Postoperative recovery was uneventful, with resolution of symptoms and no recurrence at 3-month follow-up.ConclusionAdventitial cysts of the femoral vein, though rare, should be considered in patients with unexplained limb swelling. Multimodal imaging is critical for differential diagnosis, and complete surgical excision remains the definitive treatment. This case underscores the importance of recognizing atypical venous pathologies to prevent misdiagnosis and ensure optimal outcomes.

Renal cell carcinoma (RCC) with inferior vena cava tumor thrombus (IVCTT) remains a major clinical challenge. Venous outflow obstruction from the thrombus can precipitate severe lower-extremity edema and secondary deep vein thrombosis (DVT). Current guidelines do not recommend routine placement of inferior vena cava filters (IVCFs) in this setting because progressive tumor thrombus may increase the risk of filter migration and can worsen thrombosis. Here, we report a 52-year-old man with right RCC and a level II IVCTT (Mayo classification) complicated by extensive iliofemoral DVT. He was treated using a combined interventional strategy that included endoluminal brachytherapy with long iodine-125 (^125I) seed strands, catheter-directed thrombolysis (CDT), and renal artery embolization (RAE). After treatment, inferior vena cava outflow improved markedly, and swelling of the lower limbs and scrotum resolved. Follow-up imaging demonstrated substantial regression of the tumor thrombus and a reduced renal tumor burden. To overcome the limitations of inadequate intraluminal dose coverage and the technical difficulty of safely implanting seeds directly within a mobile tumor thrombus, we used two self-designed long ^125I seed strands that were securely anchored at the jugular venous access region to deliver continuous, localized irradiation to the IVCTT. CDT and RAE were applied to further reduce thrombus and tumor volume and were associated with a favorable clinical response in this patient. The patient remained alive without disease progression for more than 39 months from diagnosis. This case illustrates the potential role of a multimodal interventional approach for simultaneous control of IVCTT and venous thrombosis and highlights the feasibility of endoluminal brachytherapy using radioactive seed strands as a strategy to manage complex RCC with IVCTT.

A previously healthy 19-year-old male presented with 1 day of transient right-sided weakness, numbness, and gait disequilibrium after recent self-limited sinonasal symptoms and minor nasal trauma with epistaxis. He was afebrile but with focal deficits, leukocytosis, and elevated C-reactive protein. Noncontrast head CT showed a left frontal lesion with vasogenic edema; MRI demonstrated a 2.4 × 1.4 cm rim-enhancing lesion in the left paramedian precentral gyrus with homogeneous diffusion restriction, low apparent diffusion coefficient, and surrounding edema. Stereotactic aspiration was performed within 24 h of presentation to obtain microbiological diagnosis and source control. A neuronavigated, transgyral frontal approach was used to avoid eloquent cortex. Empiric antimicrobials were initiated immediately after operative sampling. Postoperatively, the patient developed transient distal right lower extremity weakness that improved with supportive care and physical therapy. A thorough cardiac, dental, and thoracic evaluation did not reveal a source; the case was deemed cryptogenic. Operative cultures grew Streptococcus intermedius and Aggregatibacter aphrophilus. Targeted intravenous therapy was administered with near-complete radiographic resolution and full neurologic recovery at 4-month follow-up. This case emphasizes three practical principles for trainees: maintain suspicion for intracranial infection in afebrile young patients with new focal deficits and recent sinonasal symptoms; prioritize microbiological diagnosis and source control, while not delaying empiric therapy; and plan stereotactic trajectories that respect eloquent cortex and anticipate transient postoperative deficits. Early imaging, meticulous source evaluation and control, and directed therapy remain central to outcome.

Pleural effusions can be manifestations of heart failure, pulmonary embolism, infection, and malignancy. Symptom assessment, imaging, and pleural fluid analysis serve as key determinants in guiding clinical management. We present the case of a 75-year-old woman with a history of heart failure who developed worsening dyspnea and lower extremity edema. Initial imaging revealed a large unilateral pleural effusion, initially presumed to be secondary to heart failure exacerbation. Pleural fluid analysis demonstrated a discordant exudative effusion by Light's criteria. Following thoracentesis, the development of a tension pneumothorax improved radiographic clarity, revealing previously obscured metastatic osseous lesions that had been masked by the pleural effusion and adjacent lung parenchyma on prior imaging. This prompted further advanced cytologic evaluation which identified dysplastic breast ductal epithelial cells consistent with a malignant pleural effusion. This case underscores the importance of maintaining a broad differential diagnosis, even when pleural fluid analysis is only marginally exudative. Moreover, the occurrence of tension pneumothorax facilitated the identification of occult metastatic lesions, highlighting the essential role of post-procedural imaging in detecting concealed malignancy. This case further emphasizes that even mildly positive exudative effusions necessitate comprehensive investigation for malignancy, as subtle presentations may still indicate significant underlying pathology.

We present the case of a 79-year-old woman with new-onset nephrotic syndrome discovered by working up worsening lower extremity edema. Renal biopsy showed a pathology report consistent with minimal change disease (MCD). The patient was treated with prednisone and, subsequently, tacrolimus with good clinical response and improvement in her serum albumin and total protein levels upon outpatient follow-up. This case underscores the importance of a broad differential for the common complaint of lower extremity edema and the additional risks of MCD and adverse effects of its treatment.

Pulmonary embolism is an uncommon complication of snake envenomation. While venom-induced consumption coagulopathy typically produces hemorrhagic manifestations, thrombotic complications can paradoxically develop, requiring careful timing of anticoagulation given competing hemorrhagic risks. We report a 65-year-old woman without thromboembolic risk factors who presented 3 days after a snake bite with progressive lower limb swelling and dyspnea. Physical examination revealed unilateral edema with visible fang marks. Despite normalized coagulation parameters, markedly elevated D-dimers prompted computed tomography pulmonary angiography, which demonstrated bilateral segmental pulmonary embolism without detectable lower extremity deep vein thrombosis. The patient was treated with therapeutic anticoagulation using low-molecular-weight heparin followed by rivaroxaban for 6 months, achieving complete resolution without hemorrhagic complications. Snake venom disrupts hemostasis through a biphasic response: initial consumption coagulopathy depleting factors and platelets, potentially followed by a compensatory prothrombotic phase with hyperfibrinogenemia and thrombocytosis. Additionally, specific venom proteases directly cleave fibrinopeptides A and B from fibrinogen while activating factor XIII, creating stable cross-linked fibrin deposits resistant to fibrinolysis. The absence of deep vein thrombosis suggests thrombogenesis occurs through in situ pulmonary mechanisms or undetectable microemboli. The favorable outcome supports safe initiation of therapeutic anticoagulation once acute coagulopathy resolves. Pulmonary embolism, though rare, can complicate snake envenomation even when coagulation parameters are normalized and deep vein thrombosis is absent. After coagulopathy resolves, anticoagulation is safe. Monitoring for thromboembolic events beyond the acute hemorrhagic phase remains essential.

Papillary fibroelastoma (PFE) is a benign primary cardiac tumor arising from the endocardial surface, most commonly affecting the valvular endocardium. Although often incidental, PFEs may lead to serious complications, including systemic embolization, valvular obstruction, or regurgitation. Aortic valve fibroelastoma resulting in severe aortic insufficiency (AI) may be rare. A 77-year-old woman with a history of hypertension and chronic kidney disease presented with progressive dyspnea, orthopnea, and bilateral lower extremity edema. Examination revealed a diastolic murmur at the left lower sternal border. Transthoracic echocardiography demonstrated a tri-leaflet aortic valve with preserved left ventricular systolic function and moderate eccentric aortic regurgitation due to incomplete cusp coaptation. A transesophageal echocardiogram was performed, which revealed a small, filamentous, and mobile mass that was visualized at the base of the noncoronary cusp (NCC), consistent with a PFE. There were no clinical or laboratory findings suggestive of infection, and the lesion's morphology was inconsistent with vegetation. Holodiastolic flow reversal in the descending aorta confirmed severe AI. The patient was diagnosed with acute decompensated heart failure secondary to severe aortic regurgitation. After medical optimization, she underwent surgical aortic valve replacement. Intraoperative histopathology confirmed the presence of a fibroelastoma originating from the NCC. Postoperative recovery was uneventful, and the patient demonstrated marked symptomatic improvement. This case illustrates a rare presentation of PFE causing severe aortic regurgitation through mechanical interference with cusp closure rather than leaflet destruction. PFEs are typically small, avascular, and pedunculated, and when located near the coaptation zone, they can prevent complete leaflet closure, resulting in significant hemodynamic compromise. Echocardiography remains the diagnostic modality of choice, and multimodal imaging may aid in differentiating PFEs from vegetations or thrombi. Surgical excision is recommended for symptomatic, mobile, or left-sided PFEs due to the risk of embolization and valvular dysfunction. Although rare, PFE of the aortic valve should be recognized as a potential cause of severe AI. Early diagnosis and timely surgical management are curative and prevent embolic complications.