35-year-old patient with leg DVT



Doctor's Information

Name : Morteza
Family : Sanei Taheri
Affiliation :Radiology Department,Shohada Tajrish Hospital,SBMU
Academic Degree : Associate Professor of Radiology
Email : This email address is being protected from spambots. You need JavaScript enabled to view it.
Resident : Afarin Sadeghian


Case Section

Abdominal Imaging


Patient's Information

Gender : Male
Age : 35


Clinical Summary

35-year-old patient admitted to the hospital suffering from right leg swelling and pain with established DVT in Doppler US exam


Imaging Findings

Axial gradient-echo T2-weighted(Fig.1) and T1-weighted (Fig.2) images demonstrate low signal area in infra renal IVC in comparison with high signal flow in aorta and illiac arteries.In correlation with T2-weighted spin-echo image(Fig.3) this area show high signal intensity in comparison with normal flow void of adjacent vessels,more consistent with thrombosis.In fat-suppressed T1-weighted gradient-echo with contrast injection images(Fig.4,5,6 and 7) low signal intensity-filling defects in infra renal IVC and both common illiac veins are clearly seen.Also,subpleural consolidation in left lung base (Fig.8) is noted,suggestive of pulmonary infarct.As an incidental finding,the vertebral body lesions,high signal on T2-weighted(Fig.9) and T1-weighted(Fig.10) images are seen,most consistent with hemangioma.


Differential Diagnosis

1.Primary vein thrombosis,2.Tumoral thrombosis,3.Tumoral lesion(less likely):leiomyosarcoma


Final Diagnosis

Hyper coagulative state due to factor v Leiden with the same history in his uncle


Discussion (Related Text)

In the normal person, factor V functions as a cofactor to allow factor Xa to activate an enzyme called thrombin. Thrombin in turn cleaves fibrinogen to form fibrin, which polymerizes to form the dense meshwork that makes up the majority of a clot. Activated protein C is a natural anticoagulant that acts to limit the extent of clotting by cleaving and degrading factor V.Factor V Leiden is an autosomal dominant genetic condition that exhibits incomplete dominance,and many people carrying the mutation do not suffer any consequences. The condition results in a factor V variant that cannot be as easily degraded by activated Protein C.The excessive clotting that occurs in this disorder is almost always restricted to the veins, where the clotting may cause a deep vein thrombosis (DVT). If the venous clots break off, these clots can travel through the right side of the heart to the lung where they block a pulmonary blood vessel and cause a pulmonary embolism. It is extremely rare for this disorder to cause the formation of clots in arteries that can lead to stroke or heart attack, though a "mini-stroke", known as a transient ischemic attack, is more common .





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