98 AMERICAN JOURNAL OF OPHTHALMOLOGY July, 1988

Bright Light Stimuli as a Mask of Relative Afferent Pupillary Defects Mark Borchert, M . D . , and Alfredo A. Sadun, M . D . Department of Ophthalmology, University of South­ern California School of Medicine.

Inquiries to Mark Borchert, M.D., Massachusetts Eye & Ear Infirmary, 243 Charles St., Boston, MA 02114.

The ophthalmologist often uses the brightest available light source, including an indirect ophthalmoscope, to check for relative afferent pupillary defects. We have noted that relative afferent pupillary defects are often more obvi­ous when testing with a relatively dim light. To explore this phenomenon, we determined the effect of bright light exposure (up to levels equivalent to an indirect ophthalmoscope set at high intensity) on the pupil over varying peri­ods of time (Fig. 1). Bright light led to pro­longed pupillary miosis of five minutes' dura­tion. Reducing the intensity of the light stimulus to only 0.5 foot-candles (1/1,000 the intensity of full indirect ophthalmoscope expo­sure) for 10 "3 seconds was required to abolish this prolonged miotic effect (Fig. 2). This work is in agreement with previous studies.1

The prolonged pupillary miosis may be caused by retina bleaching or by a more com­plex neural effect. Regardless, this prolonged miosis may obscure any relative pupil dilation in the alternate light stimulation test for rela­tive afferent pupillary defects.

Additionally, an exponential decline in pu­

pillary responsiveness occurs in the miotic state.2 Stimulation with a bright light could put the pupil in this less responsive miotic posi­tion, making it difficult to assess subtle differ­ences in pupillary excursion. For practical pur­poses it is this difference in pupillary excursion that allows for the detection of relative afferent pupillary defects.

There is another theoretical advantage in using a relatively dim light to detect subtle relative afferent pupillary defects. A close cor­relation exists between the size of the relative afferent pupillary defect as measured by neu­tral density filters, and the relative visual field loss.3 Although both physiologic and anatomic studies suggest that the density of pupillomo-tor ganglion cells may be slightly higher in the macula, they are well distributed throughout the retina.31 Hence small macular lesions, even though associated with severe loss of visual acuity, have small relative afferent pupillary defects, while optic nerve lesions that produce large peripheral field loss, even in the presence of good visual acuity, have larger relative affer­ent pupillary defects.

Optimum pupillary function reflects the characteristics of the area of the retina being stimulated. For example, the pupillary reactivi­ty is lower with peripheral stimulation than with foveal stimulation, but the threshold for reactivity is also much lower.5 Additionally, the smaller peripheral responses are suppressed readily by adaptation to light. Therefore, the small relative afferent pupillary defect caused by an optic nerve lesion that results in a small

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Darkness Room light

Time after flash (seconds)

Fig. 1 (Borchert and Sadun). Exposure to bright light of 500 foot-candles for 10~3 seconds causes a prolonged pupillary miosis. The average pupil diam­eters in 14 normal subjects after exposure to a bright flash returns to the preflash baseline within five minutes in both light and dark adapted states (±1 S.D.).

Time after flash (seconds)

Fig. 2 (Borchert and Sadun). Reduction from full flash intensity of 500 foot-candles by log unit decre­ments for 10 3 seconds accelerates a return to the preflash pupil diameters. A one-thousandfold decre­ment in intensity is required to abolish the prolonged miotic effect.

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area of peripheral field loss might be masked easily by the brisk foveal reflex from bright light. On the other hand, relative afferent pu­pillary defects associated with central field loss may be more prominent with a brighter stimu­lus. Perhaps a brighter stimulus should be used after failure to demonstrate a relative afferent pupillary defect with a dim stimulus in patients with poor visual acuity.

Further studies should be undertaken to as­sess the optimum stimulus intensity for detect­ing relative afferent pupillary defects, while considering the nature of the relative field loss. In the meantime, we recommend that the clini­cian begin a pupillary examination in a dark­ened room with a dim light stimulus, before proceeding to a brighter light source.

References

1. Newsome, D. A.: Afterimage and pupillary activity following strong light exposure. Vision Res. 11:275, 1971.

2. Loewenfeld, I. E., and Newsome, D. A.: Iris mechanics. I. Influence of pupil size on dynamics of pupillary movements. Am. J. Ophthalmol. 71:347, 1971.

3. Thompson, H. S., Montague, P., Cox, T. A., and Corbett, J. J.: The relationship between visual acuity, pupillary defect, and visual field loss. Am. J. Oph­thalmol. 93:681, 1982.

4. Gamlin, P. D. R., Reiner, A., Erichsen, J. T., Karten, H. J., and Cohen, D. H.: The neural sub­strate to the pupillary light reflex in the pigeon. J. Comp. Neurol. 226:523, 1984.

5. Lowenstein, O., and Loewenfeld, I. E.: Influ­ence of retinal adaptation upon the pupillary reflex to light in normal man. Am. J. Ophthamol. 51:644, 1961.

Expulsive Choroidal Hemorrhage Following Suture Removal After Penetrating Keratoplasty Henry D . Perry, M . D . , and Eric D. Donnenfe ld , M . D . Corneal Service, North Shore—Cornell University Hospital.

Inquiries to Henry D. Perry, M.D., North Shore—Cornell University Hospital, 300 Community Dr., Manhasset, NY 11030.

Following postkeratoplasty suture removal, numerous complications that have been report­ed include wound dehiscence, bacterial en-dophthalmitis, and increased frequency of graft rejections.13 We encountered a case of delayed expulsive choroidal hemorrhage 16 months after keratoplasty following suture re­moval.

An 80-year-old man had severe ocular pain from bullous keratopathy. He previously had a cataract extraction with implantation of an Azar intraocular lens in 1983. He had hyperten­sion with chronic bronchitis.

On ocular examination on Oct. 15, 1985, the visual acuity with correction was hand move­ments in the right eye and 20/60 in the left eye. Applanation tension was 21 mm Hg in the right eye and 23 mm Hg in the left eye. The right cornea had dense bullous keratopathy and the left cornea was clear. There was a well posi­tioned Azar intraocular lens in the right ante­rior chamber. The iris was distorted superiorly. A 7.5-mm penetrating keratoplasty with an 8.0-mm donor button, anterior vitrectomy, in­traocular lens exchange, and iridoplasty was performed on Jan. 17, 1986. The suturing tech­nique used was 16 interrupted 10-0 nylon su­tures at 90% depth buried on the recipient side.

The patient did well postoperatively but had mild glaucoma. The intraocular pressure post­operatively varied between 25 and 35 mm Hg. When seen on March 9, 1987, the corneal graft was clear and compact. The intraocular pres­sure was 28 mm Hg. The patient had a treat­ment regimen of fluorometholone, pilocarpine 4% ointment at bedtime, and timolol maleate 0.5% twice daily in the right eye.

The patient returned May 12, 1987, for suture removal. His visual acuity at that time was 20/400. The intraocular pressure was 25 mm Hg and the sutures were removed according to a previously described method.4 A large wound gap was immediately noted temporally be­tween the 2 and 4 o'clock meridians. The cham­ber was still formed and deep. The patient was told another small operation was necessary to resuture the area of weakness. The patient's wife fainted and was taken out of the office in a wheelchair and rushed to the hospital emer­gency room, where it was determined she had a myocardial infarction. The patient was admit­ted two hours later. A nurse called stating the patient had a bloody drainage from his right eye and had a hypertensive crisis at that time. The patient was seen ten minutes after the telephone call and was found to have an expul-