Sava Elena A, Sântean Claudiu I, Manea Andrei, Crăciun-Ciorba Nicoleta M
Cardiology, Emergency Institute for Cardiovascular Diseases and Transplantation, Targu Mures, ROU.
Radiology, County Emergency Clinical Hospital of Targu Mures, Targu Mures, ROU.
Cureus. 2024 Oct 26;16(10):e72425. doi: 10.7759/cureus.72425. eCollection 2024 Oct.
Although thrombotic events are uncommon in young individuals, patients with genetic mutations in coagulation factors may develop extensive multisite thrombosis. We present the case of a 26-year-old patient, a smoker for nine years, who was admitted to the hospital complaining of right thigh pain with swelling, right flank abdominal pain, dyspnea, and hemoptysis. A medical history provided by the patient indicated that one month prior to presentation, an accidental fall had resulted in multiple rib fractures, bilateral hemopneumothorax, and pneumomediastinum. These injuries were treated with bilateral pleurotomy and passive pleural drainage. Upon initial presentation, the electrocardiogram (ECG) exhibited a distinctive pattern indicative of pulmonary embolism (PE), specifically sinus tachycardia and the S1Q3T3 pattern. Additionally, the thoraco-abdominopelvic angio-CT revealed acute PE in the branches of the pulmonary arteries supplying the bilateral lower lobes and deep vein thrombosis in the right external iliac vein, right common iliac vein with a protruding filling defect of approximately 18 mm in the inferior vena cava and extension to the left common iliac vein. Furthermore, a Doppler ultrasound of the right lower extremity revealed the presence of thrombosis along the entire right femoro-popliteal axis. Subsequent screening for hereditary thrombophilia revealed a heterozygous factor V Leiden G1691A* mutation and elevated levels of anticardiolipin antibodies. Despite the patient's compliance with non-vitamin K antagonist oral anticoagulants (NOACs) following discharge, a new thrombotic event, left femoral-popliteal venous axis thrombosis, occurred after a three-month interval. Repeat testing for anticardiolipin antibodies revealed an elevated titer, leading to a diagnosis of antiphospholipid syndrome. Given this diagnosis, anticoagulation with an antivitamin K was initiated. Screening for hereditary thrombophilia is crucial in young patients with thromboembolic events, as genetic causes may influence the therapeutic management and duration of anticoagulant treatment.
尽管血栓形成事件在年轻人中并不常见,但凝血因子发生基因突变的患者可能会出现广泛的多部位血栓形成。我们报告一例26岁患者,有9年吸烟史,因右大腿疼痛伴肿胀、右侧腹胁部疼痛、呼吸困难和咯血入院。患者提供的病史表明,在就诊前一个月,一次意外跌倒导致多根肋骨骨折、双侧血气胸和纵隔气肿。这些损伤通过双侧胸膜切开术和被动胸腔引流进行治疗。初次就诊时,心电图(ECG)呈现出提示肺栓塞(PE)的独特模式,具体为窦性心动过速和S1Q3T3模式。此外,胸腹部盆腔血管CT显示,供应双侧下叶的肺动脉分支存在急性PE,右髂外静脉、右髂总静脉有深静脉血栓形成,下腔静脉有一个突出的充盈缺损,大小约为18 mm,并延伸至左髂总静脉。此外,右下肢多普勒超声显示沿整个右股腘轴存在血栓形成。随后对遗传性易栓症的筛查发现了杂合子因子V莱顿G1691A*突变和抗心磷脂抗体水平升高。尽管患者出院后一直遵医嘱服用非维生素K拮抗剂口服抗凝剂(NOACs),但在三个月后仍发生了新的血栓形成事件,即左股腘静脉轴血栓形成。抗心磷脂抗体的重复检测显示滴度升高,从而诊断为抗磷脂综合征。基于这一诊断,开始使用抗维生素K进行抗凝治疗。对年轻的血栓栓塞事件患者进行遗传性易栓症筛查至关重要,因为遗传原因可能会影响抗凝治疗的管理和持续时间。