MSK for Thursday, June 4th, 2026

History

A 16 year old female presented with a symptomatic right triceps intramuscular vascular malformation. MRI demonstrated a 2.4 x 3.1 x 5.1 cm predominantly T2 hyperintense, mildly T1 hyperintense, heterogeneous enhancing mass at the mid-to-distal triceps muscle, with focal T2 hypointense areas suggestive of phleboliths. Under ultrasound guidance with a tourniquet applied to the right upper extremity proximal to the lesion, venous access was obtained, and contrast injection confirmed filling of the nidus without rapid outflow. The lesion was successfully treated with percutaneous sclerotherapy using a mixture of sodium tetradecyl sulfate (STS), lipiodol, and air. Post-intervention imaging demonstrated decreased conspicuity of the lesion with avascular ovoid regions consistent with treatment effect.

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Question

Which imaging finding most strongly supports the diagnosis of a low-flow venous malformation rather than a high-flow vascular lesion?

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Correct answer

Filling of the lesion nidus without rapid venous outflow and presence of phleboliths

Discussion

On MRI, a low-flow venous malformation typically appears as a well-defined, T2 hyperintense lesion with possible mild T1 hyperintensity and heterogeneous enhancement. The presence of phleboliths, seen as T2 hypointense foci, is highly suggestive of a venous malformation. In contrast, high-flow lesions such as arteriovenous malformations (AVMs) demonstrate flow voids, enlarged feeding arteries, and early venous drainage due to rapid shunting.

 On ultrasound and angiography, low-flow lesions show slow filling of the nidus without rapid venous outflow, whereas high-flow lesions demonstrate arterialized flow with early venous drainage. In this case, angiography confirmed filling of the nidus without outflow, consistent with a low-flow venous malformation.

 This distinction is critical for management. Low-flow venous malformations are ideal candidates for percutaneous sclerotherapy, as sclerosants such as sodium tetradecyl sulfate induce endothelial damage, thrombosis, and fibrosis, leading to lesion shrinkage while preserving surrounding tissue. In contrast, high-flow lesions require different approaches, such as embolization of arterial feeders or surgical intervention, as sclerotherapy alone would be ineffective and potentially unsafe due to rapid systemic spread.

 In this patient, the imaging and procedural findings supported a low-flow venous malformation, making ultrasound-guided percutaneous sclerotherapy the preferred first-line treatment, particularly given the intramuscular location where surgery could risk significant functional impairment.

Intramuscular venous malformations are uncommon lesions that represent diagnostic and therapeutic challenges due to their rarity, presentation, and infiltrative growth patterns. Historically referred to as intramuscular hemangiomas, these lesions are now more accurately classified under the International Society for the Study of Vascular Anomalies (ISSVA) system as low-flow venous malformations. This is an important distinction to note as management strategies differ significantly between high-flow arteriovenous malformations and low-flow venous malformations. In this case, MRI findings exhibited T2 hyperintensity, mild T1 hyperintensity, heterogeneous enhancement, and phleboliths, which are characteristic of a low-flow venous malformation.

Surgical intervention has historically been considered definitive treatment for intramuscular venous malformations. However, surgical excision may be difficult in cases with poorly defined margins or infiltration into the muscle, perhaps requiring significant removal of a muscle group. In this case, surgical intervention carried the risk of functional impairment due to the location of the lesion at the mid to distal triceps muscle. Thus, percutaneous sclerotherapy was chosen as first-line treatment for this symptomatic low-flow venous malformation. The goal of sclerotherapy is endothelial destruction leading to local thrombosis and fibrosis of the venous malformation while preserving surrounding tissue.

Several technical considerations were critical to the success and safety of this procedure. The use of ultrasound for initial guidance allowed for real-time visualization of the needle trajectory into the venous channel while avoiding adjacent arteries or nerves. Once access was obtained, a diagnostic angiogram was used to confirm the placement of the needle within the nidus of the malformation and assess venous flow. Filling of the nidus with absence of venous outflow confirmed the lesion to be a low-flow malformation, thus an ideal target for sclerotherapy. The sclerosant of choice was a foam mixture of sodium tetradecyl sulfate (STS), lipiodol, and air. This foam increases the surface area of the sclerosant, allowing it to treat a larger portion of the lesion with smaller volume of the drug. Lipiodol, with radiopaque qualities, enabled real-time fluoroscopic monitoring of the sclerosant distribution within the nidus, thus preventing non-target embolization.

Sclerotherapy may carry potential adverse effects such as post-procedural pain and swelling that can be managed with analgesics and compression. If the sclerosant extravasates, rare complications may include skin necrosis, nerve injury, or deep vein thrombosis. Thus, real-time imaging guidance and proper dosing of the sclerosant are essential to minimize morbidity.

Post-procedural imaging with ultrasound demonstrated decreased lesion conspicuity and the development of avascular ovoid regions consistent with thrombosis and fibrosis of the venous malformation. Residual heterogeneity on ultrasound may be expected early after treatment but does not necessarily indicate treatment failure. Phleboliths serve as markers of prior venous stasis.

This case highlights the potential for intramuscular venous malformations in functionally critical muscle groups to be treated without surgical morbidity. Pre-procedural imaging and flow assessment is key to understanding the type of venous malformation using the ISSVA system. Ultrasound-guided sclerotherapy allows targeted management of intramuscular low-flow venous malformation with preservation of muscle architecture and function. Long-term follow-up and assessment for recurrence risk and need for recurrent treatments is still required. It is important to note that this is a single case, and generalizability may be limited due to several factors including size, type of venous malformation, location, and functional limitations. Further prospective studies are needed to compare outcomes of sclerotherapy to surgical management for intramuscular venous malformations, specifically in the extremities.

References

• Ahmad S. Efficacy of Percutaneous Sclerotherapy in Low Flow Venous Malformations - A Single Center Series. Neurointervention. 2019;14(1):53-60. doi:10.5469/neuroint.2019.00024 Beneat A, Oropallo A. Sclerotherapy. [Updated 2024 Jan 11]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK599526/ Chen RJ, Vrazas JI, Penington AJ. Surgical Management of Intramuscular Venous Malformations. J Pediatr Orthop. 2021;41(1):e67-e73. doi:10.1097/BPO.0000000000001667 Goldenberg DC, Vikkula M, Penington A, et al. Updated Classification of Vascular Anomalies. A living document from the International Society for the Study of Vascular Anomalies Classification Group. J Vasc Anom (Phila). 2025;6(2):e113. doi:10.1097/JOVA.0000000000000113 Hein KD, Mulliken JB, Kozakewich HP, Upton J, Burrows PE. Venous malformations of skeletal muscle. Plast Reconstr Surg. 2002;110(7):1625-1635. doi:10.1097/01.PRS.0000033021.60657.74