Central venous catheters (CVCs) are essential in transplantation but can rarely fracture and embolize, with donor-to-recipient transmission of catheter fragments scarcely described. A 62-year-old woman with hepatitis C-related cirrhosis and hepatocellular carcinoma underwent orthotopic liver transplantation from a brain-dead donor with a left subclavian multi-lumen CVC in situ at procurement. Postoperative chest radiography identified a new curvilinear opacity at the left hilum, and contrast-enhanced computed tomography showed a 5 cm radiopaque structure in a segmental branch of the left lower lobe pulmonary artery, consistent with an embolized CVC tip. All recipient vascular access devices were removed intact, strongly suggesting a donor-origin catheter fragment transplanted with the liver graft. Alternative explanations, including unrecognized recipient catheter fracture and pre-existing foreign body, were considered but deemed less likely given the temporal relationship, imaging findings, and systematic device inspection. Percutaneous endovascular retrieval via femoral venous access was attempted but failed because of the fragment's distal location and probable endothelialization. Therapeutic anticoagulation was considered but not commenced because there was no radiological evidence of thrombus formation or pulmonary embolism, and substantial competing postoperative bleeding risk. The patient remained asymptomatic, and conservative management with clinical and imaging surveillance was adopted; at 6 months, she had excellent graft function and no cardiopulmonary sequelae. However, an uneventful short-term follow-up does not establish long-term safety, and early retrieval remains the preferred strategy whenever technically feasible and clinically safe. This case represents, to our knowledge, a previously unreported mechanism of donor-to-recipient CVC fragment transmission in liver transplantation, with the most plausible explanation being unrecognized transection of the donor catheter during heart procurement with subsequent lodgment in hepatic venous outflow, although definitive proof is not possible in the absence of direct intraoperative recognition. It highlights an important systems-level vulnerability at the interface between donor procurement, graft preparation, and recipient implantation. Modern multiorgan retrieval frequently involves multiple independent procedural teams, overlapping operative fields, and rapid transitions, creating fragmented responsibility for confirming removal and integrity of vascular access devices. This case underscores the importance of standardized vascular access reconciliation, careful inspection of donor venous structures, and early postoperative imaging. Structured vascular access reconciliation and verification protocols, analogous to surgical instrument counts and implant verification systems, may represent an important patient-safety intervention in transplantation.

Saddle pulmonary embolism (PE) complicated by right atrial thrombus in transit is an infrequent but highly lethal condition. Standard treatments such as systemic thrombolysis or surgical embolectomy carry significant risks, particularly in elderly or comorbid patients. We describe the case of a 76-year-old man with spina bifida, cauda equina syndrome, chronic immobility, and multiple comorbidities who presented in shock. Imaging revealed a large saddle PE with mobile right atrial thrombus and right ventricular strain. Given prohibitive surgical risk and contraindications to thrombolysis due to recent spinal infection and acute kidney injury, and high bleeding risk, he underwent percutaneous suction thrombectomy using the FlowTriever system. Large thrombus burden was successfully removed from both the right pulmonary artery and right atrium, with restoration of flow and hemodynamic stabilization. He was transitioned to long-term anticoagulation and discharged in stable condition. This case highlights the role of dual-site suction thrombectomy as a life-saving option when conventional therapies are contraindicated.

Rosai-Dorfman-Destombes disease (RDD) is a rare non-Langerhans cell histiocytosis with heterogeneous clinical presentations and an incompletely understood pathophysiology. While often indolent, a subset of patients develops aggressive, multisystem disease requiring systemic therapy, particularly in the presence of CNS involvement. We report the case of a 63-year-old male patient with disseminated RDD, including CNS lesions, marked systemic inflammation, and biclonal gammopathy at diagnosis. Initial treatment with vinblastine and dexamethasone induced complete clinical and radiological remission, which was sustained for three years under a maintenance regimen with vinblastine. Disease relapse was characterized by recurrent multisystem involvement, including pulmonary, sinonasal, and CNS lesions, and was complicated by pulmonary embolism in the absence of conventional risk factors. Retreatment with corticosteroids led to rapid clinical improvement, followed by maintenance therapy with methotrexate. This case highlights the potential role of maintenance strategies in achieving durable disease control in RDD, particularly in patients with CNS or multisystem involvement. Furthermore, the association of inflammatory, immunological, and thrombotic manifestations supports the concept of RDD as a systemic inflammatory dysregulation disorder, with implications for disease monitoring and therapeutic decision-making.

Pulmonary involvement in inflammatory bowel disease (IBD) is rare, particularly as parenchymal lesions such as masses. We report a 42-year-old woman with recently diagnosed Crohn's disease, not on active treatment, who presented with pleuritic chest pain and dyspnea. Imaging revealed a right-sided pulmonary mass in contact with the pleura and diaphragm. Initial workup excluded pulmonary embolism and infection. Bronchoalveolar lavage showed lymphocytic inflammation with negative microbiology, and autoimmune studies were unremarkable. PET-CT demonstrated no metabolic activity. Histological examination of a biopsy revealed non-necrotising granulomas with eosinophilic infiltration, without evidence of malignancy or infection. Based on exclusion and clinical context, a diagnosis of pulmonary manifestation of IBD was established. Corticosteroid therapy led to rapid clinical and radiological improvement. This case highlights the importance of considering IBD-related pulmonary disease in the differential diagnosis of lung masses to avoid misdiagnosis and ensure appropriate treatment.

Early identification of patients with acute pulmonary embolism (PE) who can be safely managed in the outpatient setting has become a central priority in contemporary clinical practice. While haemodynamic instability mandates urgent reperfusion, most patients are hemodynamically stable at admission and therefore require refined risk stratification to guide therapeutic decisions and determine the appropriate level of care. The 2019 European Society of Cardiology guidelines emphasise the importance of identifying low-risk patients who may be eligible for early discharge (within 24-48 h) and home-based anticoagulation. Over the past decade, substantial progress has been made in validating clinical, biochemical, and haemodynamic criteria capable of reliably stratifying low-risk patients. The introduction of direct oral anticoagulants further simplified anticoagulation pathways, enabling shorter hospital stays and safer outpatient management. Nevertheless, the implementation of early discharge and outpatient treatment strategies remains highly heterogeneous across countries, reflecting variations in national recommendations, healthcare system organisation, and resource availability. This review aims to synthesise the current evidence on outpatient management of acute PE, with a focus on risk-stratification strategies, cost-effectiveness considerations, and contemporary guideline recommendations.

Systemic thrombolysis is recommended for high-risk PE and select intermediate-risk patients. We assessed the robustness of RCT evidence comparing systemic thrombolytic therapy with standard anticoagulation. We systematically reviewed RCTs of intravenously administered alteplase or tenecteplase versus heparin. The primary endpoint was all-cause mortality; secondary endpoints included recurrent PE, clinical deterioration in intermediate-risk patients, and major bleeding. Fragility index (FI) or reverse FI (RFI) and fragility quotient (FQ) or reverse FQ (RFQ) were calculated to assess outcome stability. Absolute and relative risk reductions, number needed to treat (NNT), and number needed to harm (NNH) were also derived. Nine RCTs enrolling 1,682 patients met inclusion criteria. Overall, systemic thrombolysis was associated with a nonsignificant reduction in mortality (1.7% vs. 3.8%; RR 0.73; 95% CI 0.39-1.38; p = 0.33) with moderate robustness (RFI = 8; RFQ = 0.004; NNT 91; RRR 27%; ARR 2.1%). Mortality was highly fragile in high-risk PE (RFI = 0) and fragile in intermediate-risk patients (RFI = 4). Systemic thrombolysis moderately reduced recurrent PE (RR 0.42; 95% CI 0.18-0.97; FI = 5; RFQ = 0.002) and prevented clinical deterioration in intermediate-risk patients (RR 0.31; 95% CI 0.15-0.65; FI = 8; RFQ = 0.006; NNT 29; RRR 71%; ARR 3.5%). Major bleeding was robustly increased (FI = 30; RFQ = 0.001; NNH 17), mainly driven by tenecteplase (FI = 9; RFQ = 0.007; NNH 11), whereas alteplase showed no significant increase (RFI = 3). Mortality benefit of systemic thrombolysis is fragile, while major bleeding risk is robust, underscoring the limitations of current guidelines and the need for adequately powered RCTs to inform individualized treatment in high- and intermediate-risk PE.