Letters to the Journal
Vol. 104, No. 6
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2. Ganley, J. P., and Comstock, G. W.: Benign nevi and malignant melanomas of the choroid. Am. J. Ophthalmol. 76:19, 1973. 3. Arnesen, K., and Normes, M.: Malignant melanoma of the choroid as related to coexistent benign nevus. Acta Ophthalmol. 53:139, 1975. 4. Naumann, G. H. O., Hellner, K., and Naumann, L. R.: Pigmented nevi of the choroid. Clinical study of secondary changes in the overlying tissues. Trans. Am. Acad. Ophthalmol. Otolaryngol. 75:110, 1971. 5. Gonder, J. R., Shields, J. A., and Albert, D. M.: Malignant melanoma of the choroid associated with oculodermal melanocytosis. Ophthalmology 88:372, 1981.
Fig. 2 (Rolddn and associates). Polygonal, hyperpigmented cells with low chromatin nuclei and evident nucleoli (hematoxylin and eosin, x312).
foci. Calcium deposits were not found. After depigmentation of the mass with periodic acidSchiff reagent, anisocytosis, anisokaryosis, irregular mitosis, and polygonal cells with low chromatin nuclei and evident nucleoli were observed (Fig. 2). Microscopically, the tumor was of the epithelioid cell type. Also noted were moderate stromal neoangiogenesis, extensive multifocal retinal invasion with infiltration, and some embolization of the retinal vessels by neoplastic cells. The retina showed distortion, disorganization, and cystoid degeneration. Marked iris hyperpigmentation was found, and dispersed melanocytes appeared in all of the ocular structures. The diagnosis of malignant melanoma was confirmed. Gonder, Shields, and Albert 5 discussed the association between uveal melanoma and ocular and oculodermal melanocytosis. Clinicians should be aware of ocular melanocytosis (melanosis oculi) associated with malignant melanoma.
References 1. Scheffer, C. H., Binkhorst, P. G., and Hamburg, A.: Malignant melanoma of the choroid in a 2-year-old infant. Ophthalmologica 169:401, 1974.
Neisseria mucosa Endophthalmitis Keith D. Carter, M.D., Craig M. Morgan, M.D., and Michael H. Otto, M.D. Vitreoretinal Service, Department of Ophthalmology, the W. K. Kellogg Eye Center (K.D.C. and C.M.M.) and the Department of Internal Medicine, Division of Infectious Diseases (M.H.O.), University of Michigan Medical Center. Inquiries to Craig M. Morgan, M.D., Huntington Eye Associates, 1151 Hal Greet Blvd., Huntington, WV 25701. Neisseriae organisms are generally considered nonpathogenic, with the exception of Neisseria meningitidis and N. gonorrhoeae. These organisms are commonly found in the upper respiratory tract, and have been isolated from the oropharynx of healthy individuals. 1 They have rarely been reported to cause disease in humans. 2 We studied a case of posttraumatic bacterial endophthalmitis caused by N. mucosa. A 12-year-old boy sustained a penetrating injury to his left eye from a dart. The dart had previously been in his mouth. The next day he developed a foreign body sensation, photophobia, and decreased visual acuity. A daily regimen of topical corticosteroids and cycloplegics was started. Eight days later, the intraocular inflammation worsened, and he was referred to us. On examination, visual acuity was R.E.: 20/20 and L.E.: hand motions. Results of a slit-lamp examination disclosed an inferior, self-sealed, full-thickness corneal wound, a hypopyon, and 4+ cells in the anterior chamber.
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No view of the lens or retina was obtained because an extensive fibrin membrane covered all but the peripheral iris. On ultrasonography, the retina was attached. Both the anterior chamber and the vitreous cavity were aspirated, and intravitreal injections of 400 |xg of clindamycin, 2.25 mg of cefazolin, and 200 |xg of gentamicin sulfate were given. A pars plana vitrectomy was performed the next day. Inflammatory material in the vitreous prevented visualization of the retina. Intravitreal injections of clindamycin, cefazolin, and gentamicin sulfate were again given, as well as 200 fig of dexamethasone. Cultures of the intraocular aspirates grew N. mucosa, which was sensitive to penicillin. The patient was treated with intensive topical and systemic penicillin G (12 million units per day) and corticosteroids. The anterior chamber inflammation quickly decreased. One week later, the retina was still obscured because of the vitreous opacification. A complicated retinal detachment was noted two weeks later in which the retina was partially encapsulated in a cyclitic membrane. The retinal detachment was unrepairable because of marked epiretinal proliferation and necrosis. The patient's visual acuity decreased to no light perception in the left eye. Neisseria mucosa, first described by Veron, Thibault, and Second 3 in 1959, is differentiated from other neisseriae by its ability to reduce nitrate to nitrite and to gaseous nitrogen. It has also been associated with cases of meningitis, endocarditis, pericarditis, empyema, and cellulitis. 2 Treatment of this organism is similar to the treatment of other neisseriae species, although resistance to penicillin may occur. Ampicillin is usually an effective alternative. 2
December, 1987
Fluctuating Visual Loss Secondary to Orbital Emphysema Keith D . Carter, M . D . , and Jeffrey A. Nerad, M . D . Oculoplastic and Orbital Surgery Service, Department of Ophthalmology, University of Iowa Hospitals and Clinics. Inquiries to Jeffrey A. Nerad, M.D., Department of Ophthalmology, University of Iowa Hospitals and Clinics, Iowa City, IA 52242. Visual loss after orbital trauma is most frequently associated with optic nerve contusion, compression, and vascular compromise. Although orbital emphysema often accompanies fractures of the orbit, visual loss secondary to orbital emphysema is rare. Usually the intraorbital air poses no threat to vision and resolves spontaneously. A 73-year-old man fell from a ladder, injuring the right side of his head and face. He reported episodes of epistaxis and hematemesis. On examination by an emergency room physician, the patient's visual acuity was R.E.: counting fingers and L.E.: 20/20. A periorbital hemorrhage was noted in the right eye and an ophthalmologic consultation was sought. Results of an ophthalmologic examination one hour later showed a right afferent pupillary defect, significant proptosis, and decreased visual acuity to no light perception in the right eye. The patient was transferred to our facility. Thirty minutes later, visual acuity had improved to R.E.: 20/40, with no evidence of an afferent pupillary defect. There was significant proptosis, periorbital hemorrhage (Fig. 1), and marked restriction of motility in all directions. There was no evidence of subconjunctival em-
References 1. Berger, U., and Miersch, M.: Zum normalen vorkomen von Neisseria mucosa (Veron et al., 1959). Z. Med. Mikrobiol. Immunol. 155:186, 1970. 2. Davis, C. L., Towns, M , Henrich, W. L., and Melby, K.: Neisseria mucosa endocarditis following drug abuse. Arch. Intern. Med. 143:583, 1983. 3. Veron, M., Thibault, P., and Second, L.: Neisseria mucosa (Diplococcus mucosus Lingelsheim). Description bacteriologique et etude du puovoir pathogene. Ann. Inst. Pasteur Microbiol. 97:497, 1959.
Fig. 1 (Carter and Nerad). Appearance of patient on initial examination. Note periorbital swelling, hemorrhage, and proptosis of the right eye.