Central retinal artery occlusion after local anesthesia for blepharoplasty

Graefe's Archive Ophthalmology for Clinical and Experimental

Communications

© Springer-Verlag 1991 Graefe's Arch Clin Exp Ophthalmol (1991) 229:593-594

Central retinal artery occlusion after local anesthesia for blepharoplasty Rosario Brancato, Alfredo Pece, and Roberto Carassa

Department of Ophthalmology, University of Milan, ScientificInstitute H S. Raffaele, Via Olgenina, 60, 1-20132 Milano, Italy Received October 15, 1990 / Accepted March 1, 1991

A 42-year-old woman underwent bilateral periocular plastic surgery for blepharochalasis. The patient underwent a complete cardiovascular examination (ECG included) during the week before surgery and no cardiovascular affects were reported. Anesthesia consisted of an injection in the upper eyelid of 2 cc 2% lidocaine without epinephrine. No retrobulbar injections were given. At day 1 after surgery, the patient noticed a sudden drop in the visual acuity of the left eye. Her best corrected visual acuity was 2/20 (right eye) and 20/400 (left eye). Anterior segments were normal at slit-lamp biomicroscopy. The ophthalmoscopic appearance of the right eye was normal, whereas the left eye showed peripapillary and macular edema. Fluorescein angiography demonstrated the occlusion of some branches of the superotemporal and infero-temporal retinal arteries and revealed ischemia along the vascular arcades and in the macula as well as hyperfluorescence of the optic disc (Fig. 1, top). At I week thereafter, retinal fluorescein angiography showed delayed filling of the supero-temporal artery. After 3 weeks the visual acuity of the left eye had improved to 20/200. Dot hemorrhages at the posterior pole and arterial narrowing were visible. Fluorescein angiography showed persistent, delayed arterial filling and hemorrhages at the macula (Fig. 1, bottom). Acute occlusion of choroidal and retinal vessels has been reported as a rare but dramatic consequence of steroid injections in periocular or retrobulbar tissues [14] but, to our knowledge, has never been described after the injection of local anesthetics. The occlusion is due to the anatomical relation between the periocular arteries and the ophthalmic artery. In fact, when a fluid is injected into a periocular artery (ethmoidal, orbitary or lacrimal), it flows backwards and reaches the ophthalmic artery, which distributes the fluid to the central retinal artery as well as to the short posterior ciliary arteries [4]. Microemboli can be carried by retrograde transport when the injection pressure is higher than the arterial pressure. Offprint requests to: R. Brancato

Fig. 1. Top: Fluorescein angiography of the left eye at day 1 postsurgery. Bottom: At 3 weeks after surgery, the angiography shows delayed arterial filling and some dot hemorrhages at the macula

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Whereas the pathogenic mechanism is clear in the case of insoluble steroids, it is puzzling in the present case. We suppose that the fluid injected reached the palpebral portion of the lacrimal gland and induced a release of tissue substances into the lacrimal artery, resulting in their retrograde transport directly into the central retinal artery (Fig. 2). References

Fig. 2. Proposed route of the retrograde flow of glandular or periocular substances in the lacrimal artery back to the ophthalmic artery

1. Ellis PP (1978) Occlusion of the central retinal artery after retrobulbar corticosteroid injection. Am J Ophthalmol 85:352-356 2. Friedberg HL, Kline OR Jr (1986) Controlateral amaurosis after retrobulbar injection. Am J Ophthalmol 101:688-690 3. Thomas EL, Laborde RP (1986) Retinal and choroidal vascular occlusion following intralesional corticosteroid injection of a chalation. Ophthalmology 93:405 407 4. Whiteman DW, Rosen DA, Pinkterton RMH (1980) Retinal and choroidal microvascular embolism after intranasal corticosteroid injection. Am J Ophthalmol 89:851-853