Spinal Capillary and Cavernous Haemangiomas in Developmental Age: Our Experience

In 1863, Virchow proposed the first classification of vascular anomalies. He considered these lesions to be tumors (“angiomas”) and classified them into three categories (“simplex”, “cavernosum”, and “racemosum”) according to the microscopic appearance of the diseased vascular channels [2]. It was subsequently stated that angiomas could be either capillary, venous or arterial (with or without fistulae) based on the stage at which vascular morphogenesis was altered [3]. Setting aside Virchow’s hypothesis, Mulliken and Glowacki, in 1982, developed a new, “binary” classification model in which they distinguished true (1) vascular “hemangiomas”, characterized by cellular hyperplasia, from (2) vascular “malformations” which instead demonstrated vessel dysplasia with normal rates of cellular turnover. They also described the different biological behavior of the two “entities” in terms of tendency to spontaneous regression (present in vascular hemangiomas, absent in vascular malformations) [4]. This scheme was later embraced by the “International Society for the Study of Vascular Anomalies” (ISSVA) at the 1996 meeting in Rome [5], “expanded” at the 2014 ISSVA workshop in Melbourne, and last revised in 2018 (the updates were crucial to fully incorporate the genetic and histopathological advances in the knowledge of these lesions) [6,7]. Vascular tumors were divided into benign, borderline/locally aggressive, and malignant, and were also further sub-classified by pattern and location to include syndromic associations, such as PHACE (posterior fossa brain malformations, large facial hemangiomas, anatomical anomalies of the cerebral arteries, aortic coarctation and other cardiac anomalies, eye abnormalities) and LUMBAR (lower body congenital infantile hemangiomas and other skin defects, urogenital anomalies and ulceration, myelopathy, bony deformities, anorectal malformations and arterial anomalies, rectal anomalies) [7].