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Show Journal of Clinical Neuro-ophthalmology 13(4): 254--257, 1993. Iron Mydriasis Pupillary Paresis from Occult Intraocular Foreign Body Mario L. R. Monteiro, M.D., James R. Coppeto, M.D., and Jose A. A. Milani, M.D. © 1993 Raven Press, Ltd., New York Two patients presented with unilateral dilated and poorly reactive pupils and were found to have a previously unsuspected intraocular iron foreign body. Both of them had normal vision and one had normal color of the iris so that the condition was missed by several physicians. The pupils reacted normally to pilocarpine 1% and also showed response to dilute (Dol %) pilocarpine. There was no response to phospholine iodide. These findings indicate that the mydriasis was due to a local siderotic parasympathetic neuropathy of the pupil. Key Words: Mydriasis-Ocular siderosis-Tonic pupil. From the Department of Ophthalmology (MoL.RoMo, 10A.A.M.), Hospital das Clfnicas of the University of Sao Paulo Medical School, Sao Paulo, Brazil; St. Mary's Hospital (JoR.c.), Waterbury, Connecticut, U.soA. Address correspondence and reprint requests to Oro Mario L. R. Monteiro, Rua Mato Grosso, 128 conjo 51, 01239-040, Sao Paulo, Brazil. 254 The differential diagnosis of a dilated, poorly constricting pupil is extensive and includes pharmacologic blockage, midbrain lesions, and damage to the oculomotor nerve, ciliary ganglion, short ciliary nerves, or the iris (1). In 1984, Monteiro and colleagues (2) reported two patients with a fixed, dilated pupil as the presenting sign of an unsuspected intraocular foreign body and called it "iron mydriasis." They stressed that it could cause diagnostic confusion and suggested that the mydriasis could be due to synaptic or nerve terminal dysfunction (2). This paper documents two patients with this condition and presents pharmacologic evidence that the mydriasis is on the basis of a local parasympathetic neuropathy of the pupil. REPORT OF CASES Case 1 A 30-year-old man complained of a dilated right pupil. Two months previously he had felt a foreign body strike his right eye when a steel tool exploded at work. Two weeks later he noticed that the right pupil was larger than the left. He went to several ophthalmologists, but the cause of his mydriasis remained undiagnosed. On examination, visual acuity was 20/20 in each eye, although he reported a yellowish discoloration of the images seen with the right eye. In ambient light, the right pupil measured 6 mm and the left 4 mm. Both irides were light brown. The right pupil would react to only 5 mm with intense direct light stimulation, with light stimulation of the opposite eye, or with maximal near effort (Fig. 1). It measured 6 mm in the dark. The left pupil had 0 normal reactions. One drop of 0.1% pilocarpme produced constriction of the right pupil to IRON MYDRIASIS 255 FIG. 1. Case 1. Mydriasis poorly reactive to direct light stimulation in the right eye. 3 mm and did not alter the left one. Other drugs were tested at least 24 hours apart. Phospholine iodide 0.6% had no effect on the right pupil. One drop of either cocaine 5% or tropicamide 1% dilated the right pupil to 8 mm. Pilocarpine 1% constricted it to 2.5 mm. Slit lamp examination revealed a corneal scar near the limbus at the 3 o'clock meridian. There was a small hole through the base of the iris seen only with gonioscopy. No inflammatory changes were observed in the anterior chamber and the intraocular pressure was normal. Indirect ophthalmoscopy with scleral depression showed a small foreign body in the vitreous, near the pars plana. The rest of the fundus was normal. Plain radiographs also documented a foreign body. Goldmann perimetry was normal in both eyes. Amplitude of accommodation was 7 diopters in the right eye and 8 diopters in the left. An electroretinogram showed that the A and B waves measured 400 f.LV and 550 f.LV, respectively, in the right eye compared to 350 f.LV and 450 f.LV in the left. The foreign body was removed through the pars plana with a magnet. Postoperative recovery was uneventful. The right pupil gradually diminished in size and recovered its contractibility. Two months later the right pupil measured 4.5 mm and reacted to 2.5 mm with light or near stimulation. Case 2 A 26-year-old man was told by his wife that his left pupil was twice the size of his right one. He did not seek medical advice but did recall that 1 month earlier, while hammering a nail, he felt a sharp pain in his left eye. At that time he had gone to an emergency room and, aside from some ecchymosis of his eyelid, no abnormality was disclosed. One month later his wife noticed that the color of his left iris, which had always been blue, was green. Again he had no visual complaints and did not seek medical attention. Three months later he awoke with severe pain and redness in the left eye and noticed that the left pupil was not as dilated as it had been in the last 3 months. On examination his visual acuity was 20/20 in the right eye and 20/25 in the left. The right iris was blue and the left greenish-brown. The right pupil was 3 mm and normally reactive; the left pupil was 4 mm and fixed to light and near. Anterior segment examination on the left side revealed a moderate inflammatory reaction in the anterior chamber. There were no obvious injuries to the cornea, lens, or iris. Dilated examination of the fundi seemed normal, but, with the help of scleral depression, there was a suggestion of a foreign body at the pars plana at the 5 o'clock meridian in the left eye. A radiograph of the left orbit documented a foreign body, 0.5 x 2 mm in size, that was surgically removed. After surgery the eye was not treated with mydriatic or cycloplegic medications. Two days later the right pupil was 3 mm and the left 4.5 mm in ambient light. The left pupil would not react to light or near effort. One drop of either phospholine iodide 0.25% or 0.6% had no effect on the left pupil. Pilocarpine 1% caused 2 mm constriction of each pupil. There was slight improvement over the following months. One year later, the right pupil was 3 mm and the left 4 mm with normal reactions. Iris color was almost symmetrically blue. JGin Neuro-ophthalmol, Vol. 13, No.4, 1993 256 M. L. R. MONTEIRO ET AL. DISCUSSION The presence of an iron-containing intraocular foreign body causes ocular siderosis with serious damage to the eye. Iron released by the foreign body will accumulate in most of the ocular tissues, including the cornea, iris, lens, and retina (7,8). Vision is lost due to cataract, retinal degeneration, or secondary glaucoma. Clinical characteristics include a rusty color to the iris and lens capsule and degenerative changes in the retina (7). Although not a common occurrence, most ophthalmologists would suspect an intraocular foreign body in a patient with such findings, particularly the difference in color of the iris. Paralytic mydriasis has long been described as one of the findings in ocular siderosis (7). However, very little attention has been given to it as the sole presenting sign of an intraocular foreign body as described in our patients. In both of them visual acuity was normal, and in one not even a slight difference in iris color was present. This observation is, however, not new. In 1901, Vossius (3) reported one patient with unilateral fixed mydriasis that was examined by several ophthalmologists and went through extensive diagnostic procedures, including neurosurgical exploration before other signs of siderosis developed and the diagnosis was made. Black (8) in 1923, Danielson and Long (9) in 1941, and Welch (10) in 1975 also reported mydriasis as the presenting sign of siderosis. Monteiro and colleagues (2) reported two children who were referred for neurologic and neuroophthalmologic consultations due to unexplained unilateral mydriasis. They were initially considered to have tonic pupils and the diagnosis of an intraocular foreign body was only made some time later when change in the iris color developed. Both children initially denied a history of ocular injury but admitted it after the diagnosis was made, demonstrating that the diagnosis may not always be apparent by history. Vossius (3) thought that the mydriasis in patients with siderosis was due to chemical stimulation of the sympathetic nerve supply. Verhoeff (11) and Duke-Elder (6) believed that it was due to damage to the iris sphincter, since deposition of iron in the iris muscle was demonstrated (11). Monteiro and coworkers (2), however, observed that the pupil constricted to 0.5% pilocarpine eyedrops, showing that the iris muscle is able to contract. They suggested that the lesion could be either at the nerve terminals or at the synapses. The present cases were submitted to extensive pharmacologic testing. Prompt constriction to 1% / Clin Neuro-ophthalmol, Vol. 13, No.4, 1993 pilocarpine confirmed that the iris muscle is not responsible for the mydriasis. Furthermore, in our Case 1 the pupil constricted to one drop of dilute (0.1 %) pilocarpine, showing denervation supersensitivity. In both cases the pupil failed to react to phospholine iodide, a miotic that acts by inhibiting the cholinesterase enzyme, leading to accumulation of acetylcholine in the synapses where it is normally released by the nerve terminals (12). These findings demonstrated that the mydriasis is probably due to damage of the parasympathetic nerve or nerve endings. The absence of paralysis of accommodation in our Case 1 suggests that this damage occurred at or very near the iris. When confronted with a patient with a unilateral dilated and fixed or poorly reactive pupil, most physicians are concerned with the possibility of damage to the intracranial third nerve by a potentially disastrous condition, such as an aneurysm. In an otherwise healthy person, however, it would most likely be caused by pharmacologic blockage, Adie's tonic pupil, or local damage to the iris muscle (1). Pharmacologic blockage to the pupil is usually diagnosed by a careful history (1,5). Tonic pupils constrict poorly to light but usually constrict well with a near effort. Redilatation is tonic, and the pupil shows denervation supersensitivity to weak solutions of cholinergic drugs. Paralysis of accommodation is a frequent associated finding (13). Damage to the iris muscle by trauma, acute glaucoma, or iris disease is usually diagnosed by a careful ophthalmic examination. When the patient is not aware of or denies any exposure to mydriatic substances and the diagnosis is not made by history and physical examination, Thompson and colleagues (1) suggest the use of the 0.5% pilocarpine drop test. If the pupil fails to constrict, the diagnosis will be either pharmacologic blockage or damage to the iris sphincter muscle. A responsive pupil will direct the diagnosis either to Adie's pupil or damage to the intracranial third nerve. Cases of iron mydriasis can therefore lead to diagnostic confusion with third nerve lesions and with tonic pupils. In the first case, the patient may be submitted to unnecessary, expensive, and potentially dangerous neuroradiologic procedures, such as angiography. In the second case, if the patient is labeled as having tonic pupil a delay in the diagnosis of an intraocular foreign body may lead to ocular damage and visual loss due to iron deposition in the ocular tissues. In our Case 1, the diagnosis was missed by several physicians. This is understandable because iron mydriasis is usually not part of the differential diagnosis of a fixed and dilated pupil (1,4-6). Fur- IRON MYDRIASIS 257 thermore, in our cases as well as in previous ones, evidence of an intraocular foreign body was not readily present on a routine eye examination.. In many such cases, the penetration occurred around the corneoscleral limbus, leaving little or no scarring in the cornea (2). In our cases, a small hole could be visualized at the iris base only with the help of gonioscopy, a procedure that is not routinely done in such cases. The foreign body could be visualized through an indirect ophthalmoscope, but only with the help of scleral depression. Once the diagnosis is suspected, however, it can be easily confirmed on plain radiograph studies, ultrasound or high-resolution computed tomography scan. In conclusion, we believe that iron mydriasis should be included in the differential diagnosis of a dilated and fixed or poorly reactive pupil. Patients should be specifically questioned about possible foreign body trauma, and the physician should maintain a high index of suspicion to avoid a delay in the diagnosis and unnecessary investigations. REFERENCES 1. Thompson HS, Newsome DA, Loewenfeld IE. The fixed dilated pupil: sudden iridoplegia or myriatic drops?-a simple diagnostic test. Arch OphtlullmoI1971;86:21-7. 2. Monteiro MLR, Ulrich RF, Imes RK, Fung WE, Hoyt WF. Iron mydriasis. Am JOphtlullmol 1984;97:794--6. 3. Vossius A. Ober die Siderosis bulbi. Ber Dtsch Ophtlullmol Ges 1901;29:170-80. 4. Glaser JS. Neuro-ophthalmology. Hagerstown: Harper Collins; 1978:171--84. 5. Rubinfeld RS, Currie IN. Accidental mydriasis from blue nightshade "lipstick." / Clin Neuro-ophtlullmoI1987;7:34-7. 6. Duke-Elder S. System of ophtlullmology, Vol. 14. St. Louis: CV Mosby; 1971:525-44. 7. Talamo JH, Topping TM, Maumenee AE, Green WR. Ultrastructural studies of cornea, iris and lens in a case of siderosis bulbi. Ophtlullmology 1985;92:1675-80. 8. Black NM. Siderosis bulbi with dilated inactive pupil: recovery. Am / OphtlullmoI1923;6:990-s. 9. Danielson RW, Long Jc. Dilated pupils with retained intraocular steel. Am / Ophtlullmol 1941;24:330-1. 10. Welch RB. Two remarkable events in the field of intraocular foreign body: (1) The reversal of siderosis bulbi. (2) The spontaneous extrusion of an intraocular copper foreign body. Trans Am Ophthalmol Soc 1975;73:187-99. 11. Verhoeff FH. Siderosis bulbi. Br / OphthalmoI1918;2:s71-3. 12. Havener WH. Ocular pharmacology, 3rd Ed. St Louis; CV Mosby; 1976:297-8. 13. Thompson HS. Adie's syndrome: some new observations. Trans Am Ophthalmol Soc 1977;7s:s87~26. J CIill Neuro-ophthalmol, Vol. 13, No.4, 1993 |
