A 40-year-old man was admitted to our clinic with acute left flank pain. His past medical history included a right ureteral stone and intestinal injury due to a car accident. His vitals were stable, and examination revealed isolated left costovertebral angle tenderness. Physical examination revealed a height of 182 cm and a weight of 73 kg with a body mass index of 21.8 kg/m2. He was not taking any regular medications. Regarding his social history, he was a truck driver. Urinalysis revealed microscopic hematuria (5–9/high powered field). The patient’s laboratory data revealed impaired renal function (serum creatinine, 1.13 mg/dL) and raised D-dimer levels (4.9 µg/mL). Doppler ultrasonography (USG) revealed compression of the LRV between the abdominal aorta and SMA, as well as an LRVT.
Computed tomography angiography (CTA) was performed for better visualization. This revealed compression of the LRV between the aorta and the SMA with an LRVT, and the distance between the Ao and SMA at the level of the LRV was 2.5 mm (Fig. 1). Moreover, sagittal CTA showed that the angle between the Ao and SMA was 22° (Fig. 2). We also measured the peak velocity (PV) at the hilar portion of the LRV and at the LRV between the aorta and SMA using USG. The PV was 18.7 cm/s and 107 cm/s, respectively, and the ratio of PV in the LRV between the aorta-SMA portion and the hilar portion was 5.7. The pretreatment CTA revealed that the LRVT was found distal to the compression of the LRV between the Ao and SMA. Based on the above findings, the patient was diagnosed with NCS, and this was suspected to be the cause of the LRVT. Furthermore, CTA revealed bilateral PTE (Fig. 3). There were no findings of deep vein thrombosis or thrombosis other than the LRVT on USG and CTA. Therefore, the pathogenesis of PTE appears to be the LRVT. Laboratory data and imaging studies excluded the presence of other thrombogenic factors, such as malignant neoplasm, vascular malformation, trauma, heritable thrombophilia, protein C/S deficiency, and antiphospholipid syndrome. Thus, his only thrombogenic risk factor was prolonged sitting due to his job as a truck driver. Based on the above, he was diagnosed with PTE caused by LRVT.
The patient was reviewed by the cardiology team, and he was started on rivaroxaban 30 mg daily for anticoagulation. Since the PTE was mild, the cardiologists concluded that an inferior vena cava filter was unnecessary. Ten days after the initiation of rivaroxaban, a blood test revealed improvement in renal function (serum creatinine was 0.8 mg/dL) and normalization of D-dimer (1.0 µg/mL), and CTA revealed the resolution of the PTE and a decrease in the size of the LRVT (Fig. 4). Twenty days after initiation, CTA revealed complete disappearance of the PTE and LRVT (Fig. 5). Thereafter, rivaroxaban was decreased to 20 mg daily. USG and CTA, repeated 3 and 6 months later, showed no recurrence of PTE and LRVT. After carefully reviewing the patient’s history and risk factors, no other causes of LRVT after PTE were identified. And from now, there were no adverse event from the induction of rivaroxaban.