Venous thromboembolism (VTE) in athletes presents a unique clinical challenge that contradicts the traditional perception of athletes as low-risk individuals. While regular exercise mitigates cardiovascular risk and improves venous flow through frequent mobilization, injuries, inappropriate mechanics of participation, comorbid medical conditions, recreational utilization of performance-enhancing medication, and underlying thrombophilia all create unique circumstances for thrombosis in this patient population. Individual consideration of anticoagulant agent use, duration of treatment, and pauses in treatment depend on underlying bleeding and thrombosis risk and level of activity and lifestyle for each patient. Continuation of anticoagulation after return to participation in sports also requires thorough risk-benefit assessment factoring in overall health, and hinges partially on the ability to reverse the effect of anticoagulation in dire situations. Guidance about continuation of a particular sport if long-term anticoagulation is needed depends on shared decision-making about morbidity and quality of life. Adjunct methods to prevent further thrombosis and manage post-thrombotic syndrome are also important for athletic longevity. There is a growing body of literature regarding evaluation and management of athletes with thrombosis, and the authors aim to summarize recommendations as they apply to pediatric and adult athletes. However, it is noted that continued study of this topic is needed to create more generalized recommendations rather than considerations for individual patient management, as discussed within this article.

Background: Pregnancy is a well-recognized hypercoagulable state that increases the risk of thrombotic complications, most commonly venous thromboembolism. In contrast, arterial thrombosis, including acute limb ischemia (ALI), is exceedingly rare but potentially catastrophic, and no specific recommendations address its management during pregnancy. Methods: We report the clinical presentation of a pregnant woman who developed ALI during early gestation, along with a narrative review of the available literature. Results: Available evidence on ALI during pregnancy is limited to isolated case reports, predominantly occurring in late gestation or postpartum, with only two cases described in the first or second trimester, both related to popliteal artery entrapment. Cardioembolic events secondary to peripartum cardiomyopathy, often associated with preeclampsia, represent the most frequently reported etiology, whereas in situ arterial thrombosis is uncommon and typically occurs in the presence of thrombophilia or autoimmune disease. We report the first documented case of ALI in early pregnancy occurring in the absence of structural vascular abnormalities, thrombophilic disorders or identifiable cardioembolic triggers, despite the presence of multiple clinical cardiovascular risk factors. The clinical course was further complicated by preeclampsia and postpartum hemorrhage. Conclusions: This case suggests that pregnancy-related prothrombotic changes may contribute to acute arterial thrombosis even in early gestation in the presence of an increased burden of clinical risk factors. We highlight the importance of comprehensive thrombotic risk stratification and the development of evidence-based management strategies for pregnancy-associated arterial thrombosis.

Recurrent pregnancy loss (RPL) is a clinically heterogeneous reproductive disorder, and in many women the underlying mechanism remains unexplained by standard thrombophilia evaluation. Pregnancy is characterized by a tightly regulated hemostatic balance at the maternal-placental interface. Heparanase, tissue factor pathway inhibitor 2 (TFPI-2), and heparan sulfate (HS) are expressed in placental and hemostatic pathways and may contribute to coagulation-related pregnancy complications. We investigated whether the heparanase/TFPI-2/HS axis is altered in women with RPL. Blood samples were obtained from 69 women with RPL and 47 control women with at least two normal deliveries and no history of pregnancy-related vascular complications. Samples were collected at least three months after pregnancy and in the absence of hormonal therapy. Plasma and white blood cell samples were analyzed using an enzyme-linked immunosorbent assay, Western blotting, real-time polymerase chain reaction, co-immunoprecipitation, and Sanger sequencing. Mechanistic experiments using heparanase-derived peptide 16 and TFPI-2-derived peptide 6 were performed in MCF-7 and JAR cells. We found that women with RPL had increased plasma heparanase levels, heparanase procoagulant activity, HS levels, and heparanase mRNA expression compared with controls. TFPI-2 protein and mRNA expression were also elevated. The heparanase rs4693608 AA genotype was more frequent in women with RPL and, together with rs4364254 TT, was associated with increased heparanase expression and procoagulant activity. Although TFPI-2 levels were higher in RPL, co-immunoprecipitation showed reduced heparanase/TFPI-2 complex formation, suggesting impaired inhibitory regulation. HS modulated heparanase binding to TF and TFPI-2 in a concentration-dependent, bell-shaped manner. Heparanase-derived peptide 16 increased TFPI-2 expression, supporting a regulatory feedback loop. In conclusion, RPL is associated with dysregulation of the heparanase/TFPI-2/HS axis, including increased heparanase expression and activity, altered heparanase/TFPI-2 interaction, and heparanase-related genetic variation. These findings suggest a coagulation-related reproductive mechanism that may contribute to pregnancy loss and warrants validation in larger prospective studies.

Myocardial infarction with nonobstructive coronary arteries (MINOCA) is identified in approximately 5 to 10% of patients with myocardial infarction referred for coronary angiography, and it remains a working diagnosis rather than a final mechanistic one. The diagnostic challenge is greatest in young women during pregnancy and the early postpartum period. Pregnancy-related and pregnancy-amplified conditions are increasingly recognized contributors, yet direct MINOCA evidence is uneven. This review examines how hypertensive disorders of pregnancy (HDP), gestational diabetes mellitus (GDM), antiphospholipid syndrome (APS) and inherited thrombophilia, and spontaneous coronary artery dissection (SCAD) map onto distinct patterns of coronary and microvascular injury. The links between HDP or GDM and MINOCA are supported mainly by mechanistic and microvascular studies outside dedicated MINOCA cohorts. APS, by contrast, is supported by direct although limited MINOCA-specific data, and pregnancy-associated SCAD is better characterized as a cause of myocardial infarction, although only cases with less than 50% angiographic stenosis meet MINOCA criteria. Serial high-sensitivity cardiac troponin and standard acute coronary syndrome assessment remain the diagnostic foundation. Cardiac magnetic resonance, selective intracoronary imaging, and targeted antiphospholipid testing can refine mechanism assignment after stabilization. The ratio of soluble fms-like tyrosine kinase-1 to placental growth factor is established for the evaluation of suspected preeclampsia, but its relevance to coronary microvascular injury in MINOCA remains uncertain. Inherited thrombophilia testing should be individualized rather than applied routinely. The assigned mechanism should then guide antithrombotic treatment, revascularization decisions, and follow-up. Prospective phenotype-defined studies are needed before routine biomarker-driven strategies can be recommended.

Ischemic stroke under 55 years presents a distinct etiological challenge with higher prevalence of non-atherosclerotic causes. We report a fatal case of multiterritory acute cerebral infarction with bilateral middle cerebellar peduncle (MCP) T2/FLAIR hyperintensities in a 50-year-old woman, pursuing two educational objectives: (1) provide a radiological framework for interpreting bilateral MCP T2/FLAIR hyperintensities without diffusion restriction in the context of basilar occlusion; and (2) illustrate a diagnostic approach to multiterritory arterial thrombosis concurrent with systemic infection. A 50-year-old Ivorian woman with hypertension, diabetes, and severe LEAD complicated by right lower limb trophic ulcers and local infection was admitted for sudden-onset right hemiplegia (NIHSS 9) occurring one week earlier. Brain MRI showed acute infarcts in the left corona radiata and right paramedian pons, Fazekas grade 2 leukoaraiosis, a chronic callosal lesion, and symmetric bilateral MCP T2/FLAIR hyperintensities without diffusion restriction or enhancement. MR angiography revealed left M1 occlusion and absent basilar artery flow. Transthoracic echocardiography excluded intracavitary thrombus. Laboratory tests showed leukocytosis (45,190/mm[3], 90.7% neutrophils), anemia (Hb 8.1 g/dL), elevated CRP (192 mg/L), and hyperuricemia. The patient died three weeks after admission from sepsis and multiorgan failure following above-knee amputation. Antiphospholipid and thrombophilia work-up could not be completed. Bilateral MCP T2/FLAIR hyperintensities without diffusion restriction or enhancement, in the setting of basilar occlusion and longstanding leukoaraiosis, are most consistent with chronic ischemic gliosis. Multiterritory arterial thrombosis concurrent with active systemic infection should prompt immediate parallel evaluation for thromboinflammatory conditions, including urgent antiphospholipid antibody testing, before irreversible clinical decisions are made.

Congenital antithrombin III (ATIII) deficiency is a rare hereditary thrombophilia that is caused by SERPINC1 variants. Reports on KILT syndrome, which is defined by the triad of kidney anomaly, inferior vena cava (IVC) anomaly, and leg thrombosis, have been sporadic. We described the case of a 10-year-old boy with a solitary left kidney and IVC agenesis who carried compound heterozygous variants in SERPINC1. He presented with flank pain due to renal infarction and subsequently developed massive perirenal effusion. Despite anticoagulation and prolonged percutaneous drainage, the effusion persisted and was confirmed to be of lymphatic origin. Imaging revealed abnormal lymphatic flow related to venous hypertension in the renal hilum. Complete resolution of the effusion was achieved following four sessions of ethanol sclerotherapy. To the best of our knowledge, this was the first reported case of ATIII deficiency complicated by refractory perirenal lymphatic leakage. The case suggested a potential link between thrombosis and secondary lymphatic dysfunction and demonstrated the effectiveness of repeated sclerotherapy for refractory perirenal effusion. Early recognition of hypercoagulable states in children with IVC and renal anomalies is crucial for the prevention of thromboembolic events.

Thrombotic thrombocytopenic purpura (TTP), the most common type of which is immune-mediated (iTTP), is a rare, life-threatening hematologic disorder characterized by thrombocytopenia, microangiopathic hemolytic anemia, and end-organ damage. Prompt recognition and early treatment are essential for survival. Early diagnosis and initiation of treatment are critical in iTTP. Nurses play a key role in recognizing symptoms, supporting patients through treatment, and monitoring for relapse. This review outlines the pathophysiology and clinical presentation of iTTP, along with criteria for diagnosis, with an emphasis on the role of the von Willebrand factor-cleaving protease ADAMTS-13. Current evidence-based treatment strategies are discussed, including therapeutic plasma exchange and immunosuppression with corticosteroids and monoclonal antibody-based therapies. A case study of a middle-aged patient who experienced a relapse of iTTP is presented, illustrating key clinical decision points, challenges in long-term management, and the need for interdisciplinary collaboration.

Snakebites frequently cause venom-induced consumption coagulopathy (VICC). While bleeding is common, ischaemic stroke from large-vessel occlusion (LVO) is rare. The coexistence of LVO and active VICC creates a therapeutic paradox, as reperfusion therapies risk catastrophic haemorrhage. We report a woman in her mid-60s who developed left-sided hemiplegia 6 hours after a suspected viper bite. Investigations revealed profound VICC and an acute right middle cerebral artery (M1) occlusion. Due to extreme bleeding risks, standard reperfusion therapies-intravenous thrombolysis and mechanical thrombectomy-were contraindicated. Management prioritised rapid venom neutralisation using polyvalent anti-snake venom and supportive care. Once coagulation parameters normalised, cautious antiplatelet therapy was initiated, resulting in partial neurological recovery. This case highlights a rare clinical dilemma where modern stroke treatments are unsafe due to venom-induced coagulopathy, emphasising the necessity of individualised, risk-balanced management when ischaemic and haemorrhagic risks collide.