A 28-year-old male patient, with no past history of interest, consulted for a progressive, non-painful left malar tumour that had been noticed for 15 days. He had no history of local trauma. On examination, a hard lesion was palpable on the inferoexternal rim of the left orbit, approximately 1 cm in diameter, with no apparent pulsatility.

Doppler ultrasound reported an expansive, polylobulated malar lesion with partial calcification and no vascular signal. Orbital computed tomography (CT) detected a rounded, well-defined medullary lesion with trabeculated internal structure and cortical expansion without infiltration or periosteal reaction. Magnetic resonance imaging (MRI) described an expansive malar osteolytic malar lesion measuring 16x10x13mm, with well-defined sclerotic margins, absence of perilesional soft tissue infiltration and intense contrast uptake.

Given the presumptive diagnosis of a low-flow vascular lesion, and given the progressive characteristics of the lesion, it was decided to excise the lesion under general anaesthesia. The lesion was exposed through a left subciliary approach with tail enlargement towards the malar and dissection in planes. After a box osteotomy including a peripheral safety margin of 0.5cm, the defect was reconstructed with chin graft and arched titanium plate. The intercortical gaps were filled with cancellous bone obtained from the donor site. Postoperative radiological controls showed an anatomical reconstruction with good bone consolidation.

Pathological examination revealed dilated vascular spaces lined with endothelium without atypia, concluding an "intraosseous haemangioma". However, the immunohistochemical study was negative for GLUT-1. Therefore, we consider that the correct clinical and immunohistochemical diagnosis is intraosseous venous malformation.
After 5 months of follow-up, the patient is completely asymptomatic, with an excellent cosmetic result.