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Show Journal of Clmical Nfuro- ophthaimoioxy 12( 1): 41- 42, 1992. Pain Upon Eye Movement Following Digoxin Absorption Andre Merrnoud, M. D., Avinoam B. Safran, M. D., and Noemi de Stoutz, M. D. 1992 Raven Press, Ltd., New York A patient who had received digoxin for 6 months experienced glare and ocular pain induced by eye movement. The symptoms lasted for 2 days and disappeared within hours after the treatment was discontinued. Four months later, digoxin was readministered. After 2 days, the symptoms reappeared but disappeared again within hours of stopping treatment. The origin of the pain is uncertain, although mechanisms related to optic nerve or ocular muscle involvement should be considered. Digoxin toxicity should be included in the differential diagnosis of pain evoked by ocular movements. Key Words: Digoxin- Glare. From the Neuro- ophthalmology Unit, Department of Ophthalmology, Geneva University HospitaL CH- 1211 Geneva 4, Switzerland. Address correspondence and reprint requests to Dr. A. Mermoud, Jules Gonin Eye Hospital Department of Ophthalmology, Lausanne University, Av. de France 15, CH- lO04 Lausanne, Switzerland. 41 Cardiac glycosides have been known for decades to induce toxic changes in the eyes and vision. Common side effects include glare, disturbance of color vision, and flickering of light ( 1-- 4). Temporary reduction in visual acuity is less common. Diplopia and ptosis have occasionally been mentioned in association with digitalis treatment, but these conditions may have been coincidental ( 1- 5). We recently examined a patient with a history of repeated episodes of glare and ocular pain when moving the eyes. The symptoms occurred following digoxin intake and immediately resolved upon discontinuation of the treatment. Pain induced by eye movements has apparently not been reported in association with cardiac glycoside intoxication. CASE REPORT A 32- year- old woman suffering from truncus arteriosus communis type IV according to the classification of Collett and Edwards ( 6,7) was treated from the age of 8 to 16 with digoxin 0.25 mg four times daily. When she was 25 years old, weighing 56 kg, she received digoxin 0.25 mg daily because of heart failure, After 6 months of treatment, she began to experience deep orbital pain on both sides when moving the eyes in association with a glare phenomenon. The symptoms lasted 48 hours. Treatment was then discontinued, and less than 1 day later, all symptoms had disappeared. Sixteen weeks later, digoxin 0.25 twice daily was prescribed because of a recurrence of heart failure. After 2 days of treatment, the patient experienced dazzling and orbital pain on moving the eyes. Treatment was immediately interrupted, and the ocular symptoms disappeared within hours. No ophthalmological examination was performed during these events, nor were serum digoxin levels determined. 42 A. MERMOUO ET AL. At the age of 32 at the request of the patient, who now is a physician, an attempt was made to explain these symptoms by administering digoxin 0.25 mg twice daily. Her body weight was still 56 kg. An ophthalmological evaluation performed before treatment showed 20/ 20 best corrected visual acuity in both eyes, normal fundi and ocular pressure, and full visual fields when evaluated by means of Goldmann kinetic perimetry. PatternVER and visual contrast sensitivity ( assessed by Nicolet CS 2000) were within the normal range. Three and four days after starting treatment, a reassessment of visual function showed reduced contrast sensitivity values. The patient declined electroretinography. Treatment was stopped, and tests given 1 week later showed that contrast sensitivity had returned to normal. At no stage of the therapeutic trial did the patient demonstrate any significant change in visual acuity, visual fields, pattern- VER, or fundus appearance. She did not experience color hallucinations, glare, or ocular pain. Serum digoxin level on the third day was found to be 1.58 mmoUI. Serum sodium and potassium levels were within the normal range. DISCUSSION This patient twice experienced dazzling and pain induced by eye movement during digoxin treatment. The ocular symptoms ended hours after therapy was discontinued. Despite the fact that these symptoms did not recur after a third therapeutical trial, this history strongly suggests a causal relationship between digoxin intake and the reported symptoms. Dazzling is a common complaint of patients taking cardiac glycosides and has been noted either before, or in association with, a reduction in visual acuity ( 4). In affected patients, an alteration in visual function is generally attributed to changes in receptor cells of the retina ( 5,8,9). Involvement of the optic nerve in digoxin intoxication has also been suggested ( 1,2), but we cannot be certain that this actually occurs. It has been argued that absence of disc pallor, an alteration in electroretinographyin patients receiving digoxin, and higher digoxin levels in the retina than in the optic nerve in guinea pigs receiving digoxin ( 8,9) support the existence of retinal rather than optic nerve involvement in visual disturbances caused by cardiac glycosldes. The origin of our patient's ocular pain induced by eye movement, is uncertain. Two hypotheses may be considered. First, considering that the patient showed changes in visual function and that pain on eye movement occurs with retrobulbar neuropathy ( 10) it is possible that the pain was related to optic nerve involvement. This, however, seems unlikely. While pain on eye movement is typically associated with retrobulbar neuritis ( 10), it has apparently not been reported in optic neuropathy from toxic causes. It is also conceivable that ocular pain resulted from extraocular muscle involvement ( 11), but few cases of ocular muscle changes caused by cardiac glycoside toxicity have been described. There have been two reports of ptosis and diplopia that occurred in association with the intake of cardiac glycosides ( 12,13). In these cases, however, ophthalmoplegia was probably neurogenic rather than myogenic in origin. Moreover, these patients did not report pain on eye movement. We are not aware of any reports of myalgia or myositis occurring in conjunction with treatment with cardiac glycosides. Digoxin intake may cause ocular pain on moving the eyes and should be considered in the differential diagnosis of this condition. REFERENCES 1. Wagener HP, Smith HL, Nickeson RW. Retrobulbar neuritis and complete heart block caused by digitalis poisoning. Arch Ophthalmol 1946; 36: 478- 83. 2. Sykowski P. Digitoxin intoxication resulting in retrobulbar optic neuritis. Am J Ophthalmol 1949; 32: 572- 4. 3. Robertson OM, Hollenhorst RW, Callahan JA. Receptor tunction in digitalis therapv. Arch OphtlwlmoI1966; 76: 852- 7. 4. Robertson OM, Hollenhorst RW, Callahan JA. Ocular manifestation of digitalis toxicity. Arch Ophtha/ mol 1966; 76: 640-- 5. 5. Weleber RG. Shults WT. Digoxin retinal toxicity: clinical and electrophysiologic evaluation of a cone dysfunction syndrome. Arch OphthalmoI1981; 99: 1568- 72. b. Yoshizato T. Julsrud PR. Truncus arteriosus revisited: an angiographic demonstration. Pedzatr CardioI1990; 11: 36- 40. 7. Calder L, Van Praagh R, Van Praagh S, et al. Truncus arteriosus communis. Am Heart r 1976; 92: 23-- 38. 8. Duncker G. Herzig A. On the ocular distribution of cardiac glvcosides in guinea pigs following acute administration. Graefe's Arch Clill OphthalmoI1989; 227: 55- 9. 9. Binnion P, Frazer G. Digoxin in the optic tract in digoxine intoxication. rCardiol'asc Pharmaco/ 1980; 2: 699- 706. 10. Perkin GO, Rose Fe. Optic nellritis and differential diagnosis. Oxtord: Oxford University Press, 1979: 34. 11. Spoor Te. Hartel We. Orbital myositis. r Clin Nellroophthalmol 1983; 3: 67- 74. 12. Ross JVM. Visual disturbances due to the use of digitalis and similar preparations. Am JOphthalmolI950; 33: 1438- 9. 13. Gillette OF. Visual disturbances due to digitalis. Trans Am Ophthalmol Soc 1946; 44: 156- 64. |