Neuroradiology

Ocular Complications of Orbital

Venography 1

Jan N. Safer, M.D., and Pierre Gulbor, M.D. Three ocular complications directly related to orb ital venography are described, one resulting in permanent loss of vision,. This patient had a lymphangioma of the orbit which evidently had bled secondary to increased venous pressure and injection of contrast bolus. Both of the 2 patients with transient visual disturbances had diabetic retinopathy . The common factor is felt to be an impaired vascular bed which cannot meet the stress of increased venous pressure and contrast medium injection. Conditions which predispose to ocular-orbital stasis and/or hemorrhage are discussed. INDEX TERMS:

Angiography, complications • Orbit. neoplasms • Orbit, radiography

Radiology 114:647-648, March 1975

occur. The ocular-orbital vascularity may be altered by venous perfusion of contrast material into the orbit. Stasis and/or hemorrhage may be secondary to this alteration when the vascular integrity is challenged in patients with retinal vascular disease. The radiologist should first evaluate the integrity of the ocular-orbital vascular system of the patient who is about to undergo orbital venography.

combined study to evaluate patients with uni-

A lateral exophthalmos was instituted by a neuro-

radiologist and an ophthalmologist in 1969. The accuracy of orbital venography via the percutaneous and transjugular routes has been documented by previous investigators. The purpose of this study was to correlate orbital venography with the clinical surgical findings in conjunction with time amplitude ultrasonagraphy (TAU), orbital thermography, technetium-99m orbital scans and conventional radiographic studies. Correlation with these other modalities will be reported separately. The ophthalmic complications of orbital venography have not been previously documented in the literature (1, 2). By increasing the intracranial and intraorbital venous pressure by either the percutaneous or transjugular approach, specific ophthalmic hemostatic alterations

Fig. 1.

METHOD

A pillow was placed beneath the supine patient's shoulders to lower the head. A blood pressure cuff 3 inches (7.6 cm) wide was placed around the neck and inflated to 40-50 mm Hg. After routine preparation of the skin. the head was hyperextended and a midline

Right upper lid distended by hematoma. Fig. 2. Widely dilated right pupil.

"From Wills Eye Hospital, Philadelphia, Pa. (P. G.); Temple University Hospital, Philadelphia (J. N. S.); and Manhattan Eye. Ear and Throat Hospital, New York City (P. G.). Accepted for publication in October 1974. Presented at the Tenth Symposium Neuroradiologicum, Punta del Este. Uruguay, March 10-16, 1974 shan

647

648

JAN

N. SAFER AND PIERRE GUIBOR

Table I: Conditions Associated with Ocular-Orbital Stasis and/or Hemorrhage Diabetic, arteriosclerotic or hypertensive retinopathy Central retinal artery or vein occlusion Arteriovenou s comm unications Angiomas, hemangiomas, lymphangiomas (involving orbit, choroid, retina, vitreous) Blood dyscrasias Hyperviscosity states (e.g., sickle cell, polycythemia) I ncreased bleeding tendencies

vein of the forehead was punctured with a 23-gauge "butterfly" (pediatric scalp vein) needle. At times, a compression band was applied to the scalp to achieve better venous distension. Puncture was successful in 85 % of attempted cases. Patency was maintained with intermittent saline flushing. For filming, Renografin-60 or Conray-60 in a 20-ml syringe was injected over 15 seconds while the patient applied digital pressure to the external facial veins. Films were exposed at 0, 5, 10 and 15 seconds. Ten to 12 ml of contrast agent was usually injected during this interval. Filming was done in the base, Water's, and lateral views. At times, in order to better see the veins of one side in the lateral projection, an additional injection was done while compressing the external facial vein on one side and the superior orbital vein on the other. CASE REPORTS

During the course of this investigation, 52 patients with unilateral exophthalmos of nonthyroid etiology were studied with percutaneous orbital venography. Three complications were directly related to the study. CASE I: A 56-year-Old black male with diabetes and hypertension presented with unilateral exophthalmos. He reported loss of vision of the right eye immediately following percutaneous frontal vein orbital venography with the usual jugular and external facial vein compression. The involved eye was tested immediately by the ophthalmologist and found to have no light perception for five minutes but vision gradually returned to 20/20 within six hours. Immediate funduscopic examination of the retina following the loss of vision revealed a markedly dilated central retinal vein with associated central retinal artery spasm. Some mild retinal edema was present. This patient had minimal arteriosclerotic retinopathy with arteriovenous nicking and narrowing of the arterial caliber. The associated loss of vision was probably due to an induced central retinal artery occlusion from venous dilatation at the level of the optic disc. The patient was placed on systemic prednisone (80 mg daily) and the unilateral exophthalmos abated in two weeks. The diagnosis was felt to be a clinically confirmed orbital pseudotumor. CASE II: A 62-year-old white man with bilateral Grade II diabetic retinopathy presented with unilateral exophthalmos of the left eye. Percutaneous frontal vein orbital venography was performed without complication and showed an anteriorly located mass of the orbit. No visual complaints were noted during the procedure. However, the vision in the left eye had changed from 20/30 to 20/70 on examination one week later. Funduscopic examination now revealed a new inframacular retinal hemorrhage resulting in decreased vision. In six weeks the hemorrhage was resorbed and vision returned to 20/30. Subsequent surgery revealed the mass to be a neurilemmoma. CASE

III:' A 16-year-old white girl was admitted for evaluation of

March 1975

unilateral right exophthalmos. There were no objective or subjective signs of a bruit, nor any clinical indication that an arteriovenous malformation existed in the right orbit. Visual acuity of the right eye was 20/20. Percutaneous orbital venography was performed in the usual manner, including jugular compression. The patient complained of severe pain in the right eye during injection of the contrast bolus. Only one injection was made. The upper lid became distended (Fig. 1). A large hematoma of the orbit was diagnosed secondary to massive retrobulbar hemorrhage. The involved eye had no light perception and the pupil was widely dilated (Fig. 2) with no response to light stimulation. There was no retinal edema and no apparent abnormality of the retinal arteriovenous system. Vision in the right eye never returned to normal and there was also permanent disturbance of the extraocular muscle movements. Permanent loss of vision and decreased mobility of the proptotic eye were secondary to a massive orbital hemorrhage. Subsequent carotid arteriography revealed a lymphangioma of the right orbit which evidently had bled secondary to the in'creased venous pressure and injection of contrast agent.

DISCUSSION

These three documented ocular complications associated with orbital venography appear to be directly related to the sudden increased venous pressure in the presence of contrast agent. In this work, the antegrade percutaneous injection technique was employed. We would suggest that the transjugular catheter approach to the retrograde injection of contrast material to the ocular-orbital venous system has potentially the same hazards because of the sudden increase in venous pressure induced at the time of injection, again in the presence of contrast material. The common factor is an impaired vascular bed which cannot meet the stress of the increased venous pressure and contrast agent. A complete examination should carefully evaluate the potential for possible ocular-orbital stasis and/or hemorrhage. Those ophthalmologic conditions with retinal vascular changes which predispose to ocular-orbital stasis when challenged by increased venous pressure and contrast substance are listed in TABLE I. Diabetic, arteriosclerotic and hypertensive retinopathy, which may occur in combination, all predispose to friable blood vessels with increased perfusion. Arteriovenous communications of the retina and orbit are found in higher incidence when such lesions are known to be present elsewhere in the body. The same increased incidence is seen with hemangiomas (cutaneous and ophthalmologic) and lymphangiomas. Hyperviscosity states would appear to raise the risks, again because of the heightened possibilities of stasis. The tendency toward bleeding makes it difficult to perform the procedure, and increases the possibility of hemorrhage. RadiologyGroup of New Brunswick, P. A. 303 George Street New Brunswick, N. J. 08901

REFERENCES 1. Lombardi G. Passerini A: Venography of the orbit: technique and anatomy. Br J RadioI41:282-286, Apr 1968 2. Hanafee WN: Orbital venography. Rad Clin North Am 10:6381, Apr 1972