Orbital lesions ii

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Orbital lesions ii

  1. 1. HEAD AND NECK IMAGING EHAB ABOU ELFOTOUH. MD.
  2. 2.  Orbital Varices.  Increased antero-grade flow, can result from vascular malformations of the face and scalp.  Obstruction of distal venous drainage, as cavernous sinus thrombosis.  Ab-normal retro-grade flow, as carotid–cavernous fistula.  Increased intracranial pressure.  Normal variant.
  3. 3.  Most common cause of spontaneous orbital hemorrhage.  Lesions result from congenital weakness in post-capillary venous wall.  Have a large communication with the venous system and distend during maneuvers that increase venous pressure.
  4. 4.  Have only a small communication with the venous system and do not distend.  Patients with usually manifest stress or painful proptosis.
  5. 5.  CT images:  Normal appearance, axial on supine position.  Or mild enlargement of the involved veins.  Increases venous pressure is required to demonstrate lesion distensibility.
  6. 6.  Varices may be smooth club-like, triangular, or segmental dilatation of Opth. veins.  Orbital mass of vessels.
  7. 7.  At MR imaging:  Hypo- to hyper- intense signal on T1.  Hyper-intense signal on T2.  Intense enhancing pattern.
  8. 8.  Fed by ophthalmic artery branches.  Consist of multiple congenital micro-vascular connections between arteries and veins.  Manifest with peri-orbital swelling, dilated retinal veins, visible or palpable pulsations, an audible bruit, glaucoma, and, visual field defects.
  9. 9.  Oculocerebro-cutaneous syndrome.  Consists of unilateral AVM of the visual pathways and midbrain.  Facial vascular nevi or telangiectasias.  Patients present with intracranial hemorrhage, optic atrophy and pulsatile exophthalmos.
  10. 10.  Abnormal communication between the cavernous sinus and one or more branches of the internal or external carotid artery.  Causes direct trauma, surgery, dural sinus thrombosis, or spontaneously.  Spontaneous with Ehlers-Danlos syndrome and osteogenesis imperfecta.
  11. 11.  Manifest with the classic triad of pulsatile exophthalmos, conjunctival chemosis, and an auscultatory bruit.  Gradual decrease in visual acuity.  Palsy of cranial nerves III, IV, V, and VI.
  12. 12.  CT or MR imaging:  Proptosis.  Extraocular muscle enlargement.  Superior ophthalmic vein distention.  Cavernous sinus dilatation .
  13. 13.  Intracanalicular ophthalmic artery aneurysms are extremely rare.  More common carotid-ophthalmic artery aneurysms.  Arise at origin of the ophthalmic artery.  May extend intra-cranially above the sella and sometimes extend into or through optic canal.  Lesion withdiameter of 2–3 mm are usually asymptomatic.  More than 3 mm may compress the artery or optic nerve or rupture.

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