Vascular anomalies are comprised of two main types: vascular tumors, which include infantile hemangioma and other rare vascular tumors in both children and adults, and vascular malforma­tions [1]. Vascular tumors are differentiated from vascular malformations based on the clinical appearance, imaging, and pathologic characteris­tics [2]. Examples of vascular tumors include infantile hemangioma, congenital hemangioma (rapidly involuting congenital hemangioma (RICH), partially involuting congenital heman­gioma (PICH), or non-involuting congenital hemangioma (NICH)), kaposiform hemangioen-

pathological fractures. AVMs affecting bones can sometimes result in osteolytic lesions due to the presence of periosteal and intraosseous nidus (nest) or large draining venous channels after the nidus.

This method was previously considered of lim­ited interest, even with enhanced contrast, as it only provides information on whether a lesion is highly vascularized or not. However, precise delineation and diagnosis of soft tissue lesions remain challenging, except for macrocystic LMs, where cysts are clearly depicted. The presence of phleboliths may indicate a diagnosis of venous malformation, as distinctive calcications develop on thrombosis and debris resulting from slow ow. Bony displacement or alteration can also be seen due to long-term compression in both VMs and LMs. Pathologic fractures and absorption may be observed in bone or bone­adjacent AVMs. Currently, the less invasive 4D CT has replaced angiography and can contribute to therapeutic planning and post-therapy assessment.

location, arterial supply, draining veins, and rela­tionship with normal neighboring arteries and veins. Angiography is also used for diagnosing quiescent AVMs, which may mimic a capillary malformation. However, with the current advancements in technology, 4D CT imaging can often replace angiography for pretreatment assessment with less invasiveness and greater accuracy.

as a clinically destructive sign. With a mean fol­low- up of 4.6years, the cure rate for AVMs was 75% for stage I, 67% for stage II, and 48% for stage III [6]. AVMs can worsen after trauma, hor­monal changes, pregnancy, or puberty. Duplex ultrasonography, as well as clinical signs and symptoms, can assist in the therapeutic decision­making process. However, a more precise and effective evaluation using contrast MRI, 4D CT, and angiography is necessary. While MRI pro­vides information on the spatial relationship between the lesion and surrounding tissue and organs, 4D CT and angiography are most useful for abnormal vascular assessment and therapeu­tic evaluation during embolization, which is often required to eliminate the nidus, ow, pooling, and drainage patterns around the lesion. When the AVM lesion is localized, as is often seen in stage II, and to protect vital organs, surgical removal alone or combined with prior embolization within 24–48h is the preferred rst choice. If the defect is large, reconstruction will follow [7]. If the lesion is extensive and destructive (stage III) and the margin of the lesion is unclear, controlled reduction of the lesion should be considered. Embolization to control ow supply and drainage and subsequent percutaneous transcutaneous ultrasonic-guided sclerotherapy within 24–48 h may result in sufcient reconstruction of the wound bed (Fig.4.3).