High-flow supraorbital arteriovenous malformation following trauma: A rare cause of ptosis

Post-traumatic arteriovenous malformations (AVMs) of the supraorbital region are rare but potentially serious high-flow vascular lesions. We report the case of a 46-year-old female with a 10-year history of a forehead swelling that showed rapid enlargement over the past 4 months following blunt trauma. Clinical examination revealed a large, compressible, pulsatile swelling over the frontal and right supraorbital regions with palpable thrill, audible bruit, and prominent venous engorgement. The patient also had left eye mechanical ptosis and facial asymmetry. Features suggestive of a high-output cardiac state were noted. Doppler ultrasonography confirmed a high-flow AVM, and the patient was referred to a higher center for definitive management. This case emphasizes the importance of early diagnosis of post-traumatic AVMs to prevent progression and systemic complications.

Case

A 46-year-old female homemaker presented with a progressively enlarging swelling over the left supraorbital and frontal regions, initially noticed 10 years earlier following blunt trauma from a bamboo stick. The lesion was insidious and slowly progressive for several years but exhibited rapid enlargement over the preceding 4 months. This was accompanied by pulsation, localized warmth, intermittent throbbing, and a subjective “whooshing” sound suggestive of turbulent blood flow. Over the past 3 months, she developed progressive drooping of the left upper eyelid without visual impairment. She denied pain, bleeding, ulceration, diplopia, or neurological deficits but reported mild exertional palpitations and easy fatigability. There was no history of prior vascular anomalies or similar conditions in the family. On examination, a 5–7 cm ill-defined, lobulated, compressible swelling was observed over the left frontal and supraorbital regions, extending laterally and partially crossing the midline. The lesion had a characteristic “bag of worms” appearance with prominent dilated veins, increased local temperature, expansile pulsations, palpable thrill, and a continuous bruit [Fig. 1]. It refilled rapidly after compression, and proximal arterial compression resulted in a reduction in size and pulsatility, with a positive Nicoladoni–Branham sign. Ophthalmic evaluation revealed mechanical ptosis with mild inferolateral displacement of the globe, while visual acuity and extraocular movements were preserved. Systemic examination demonstrated tachycardia and bounding peripheral pulses, suggestive of a hyperdynamic circulatory state.

Findings and Management

Color Doppler ultrasonography demonstrated a heterogeneous lesion composed of multiple tortuous vascular channels with high-velocity arterial flow and arterialized venous waveforms, along with turbulent bidirectional flow, consistent with a high-flow vascular malformation [Fig. 2]. Clinically, the presence of pulsatility, compressibility, thrill, bruit, and a positive Nicoladoni–Branham sign further supported the diagnosis of a significant arteriovenous shunt with substantial hemodynamic burden. No evidence of intraorbital extension was identified. Based on the clinical and radiological findings, a diagnosis of post-traumatic high-flow supraorbital arteriovenous malformation was established. The patient was planned for multidisciplinary management, with definitive treatment aimed at obliteration of the nidus and reduction of venous hypertension, typically through staged endovascular embolization followed by surgical excision where feasible, in order to minimize recurrence and prevent progression or systemic complications.

What is your Next Step?

1. Immediate surgical excision

2. Contrast-enhanced CT/MR angiography followed by digital subtraction angiography

3. Observation and periodic follow-up

4. Initiation of systemic corticosteroids.

Diagnosis

Post-traumatic supraorbital AVM.

Correct Answer

B.

Discussion

AVMs are high-flow vascular anomalies defined by direct communication between arterial and venous systems without an intervening capillary bed, traditionally considered congenital in origin but increasingly recognized to be influenced by external triggers such as trauma, which may precipitate the expansion of a previously dormant nidus.[1] In the craniofacial region, these lesions often remain clinically silent until stimulated by hormonal or environmental factors, after which they may present with characteristic features including swelling, pulsatility, thrill, bruit, and localized warmth; however, presentation with ptosis is distinctly uncommon and likely reflects local mass effect, venous congestion, or periocular vascular involvement. The present case represents a high-flow soft-tissue AVM, with imaging playing a central role in both diagnosis and hemodynamic characterization. Color Doppler ultrasonography serves as an essential first-line modality, demonstrating increased systolic and diastolic velocities in feeding arteries, arterialization of draining veins, and turbulent bidirectional flow patterns, while advanced imaging techniques such as contrast-enhanced computed tomography, magnetic resonance imaging, and digital subtraction angiography further define lesion extent, vascular architecture, and flow dynamics critical for therapeutic planning.[1] Craniofacial AVMs may lead not only to progressive local deformity and functional impairment but also to serious systemic complications, including high-output cardiac failure due to persistent arteriovenous shunting.[2] Management remains challenging owing to the infiltrative nature, complex angioarchitecture, and high recurrence rates of these lesions; optimal treatment strategies emphasize complete eradication of the nidus and reduction of venous hypertension, most commonly achieved through staged approaches involving endovascular embolization followed by surgical excision when feasible, as incomplete treatment is associated with recurrence and progression.[3] This case highlights that a progressively enlarging pulsatile supraorbital swelling following trauma, particularly when accompanied by characteristic vascular signs such as thrill and bruit, should raise suspicion for an underlying high-flow arteriovenous malformation. Early vascular imaging and multidisciplinary evaluation are essential to prevent local progression and systemic complications.[1,3]

The concordance between the clinical vascular signs and imaging findings established the diagnosis of a high-flow arteriovenous malformation and highlights the importance of early vascular evaluation in such presentations.

Funding Statement

Nil.