TABLE. Clinical Data of Patients in Whom a Traumatic Full-thickness Macular Hole Disappeared
Size of Macular
Duration of Macular Hole
Positive Positive Positive
20/20 20/20 20/20
4 4 3
1,RE 2, LE 3, RE
12, M 18, M 19, M
Baseball injury Traffic accident Baseball injury
20/40 20/40 20/100
0.1 0.1 0.1
* Best-corrected visual acuity. ♦Patient's report of a total interruption of a fine slit beam focused over the center of the fovea. DD = disk diameter.
for the disappearance included epiretinal membrane formation2'4; reattachment of the operculum after complete vitreous detachment4; or tissue proliferation, possibly by glial cells, retinal pigment epithelial cells, or both at the base of the hole.4 Unlike patients with idiopathic senile macular holes in which cortical vitreous may play an impor tant role in the formation and progression of the holes, there was no prefoveolar condensation of the vitreous or epiretinal membranes in our young pa tients. The lack of condensation of the vitreous may have prevented the holes from enlarging. Although the mechanism of hole disappearance in our patients is unclear, the absence of epiretinal membranes may suggest an important role for glial cell proliferation, which is likely to be vigorous in younger patients. This mechanism is consistent with the histopathologic study of the idiopathic macular hole closed after vitrectomy, that is, a defect in the fovea was bridged by glial cells.5 It is important to recognize that small traumatic macular holes in young patients can resolve spontaneously. Close observation, rather than surgi cal treatment, is recommended in these cases. REFERENCES 1. Nunode Y, Tokuoka S, Nakajima M, Watanabe C. A case of traumatic macular hole with interesting course. Jpn Rev Clin Ophthalmol [Ganka Rinsho Iho] 1983;77:922-924. 2. Lewis H, Cowan G, Straatsma BR. Apparent disappearance of a macular hole associated with development of an epiretinal membrane. A m J Ophthalmol 1986;102:172-175. 3. Guyer DR, de Bustros S, Diener-West M, Fine SL. Observa tions on patients with idiopathic macular holes and cysts. Arch Ophthalmol 1992;110:1264-1268.
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4. Yuzawa M, Watanabe A, Takahashi Y, Matsui M. Observation of idiopathic full-thickness macular holes: follow-up observa tion. Arch Ophthalmol 1994;112:1051-1056. 5. Rosa R H Jr, Glaser BM, de la Cruz Z, Green WR. Clinicopathologic correlation of an untreated macular hole and a macular hole treated by vitrectomy, transforming growth factor-B2, and gas tamponade. A m J Ophthalmol 1996;122: 853-863.
Hyperplastic Persistent Pupillary Membrane Talia Kolin, MD, and A. Linn Murphee, MD PURPOSE: To report a child with extensive bilat eral hyperplastic pupillary membranes and good visual acuity. METHOD: We examined a 9-year-old child with bilateral hyperplastic persistent pupillary mem branes present since birth. RESULTS: The patient had a visual acuity of BE, 20/30, stereopsis of 50 seconds of arc, orthophoria, and normal extraocular movements. The remainder of the ophthalmic examination was normal. CONCLUSION: Patients with bilateral hyperplas tic pupillary membranes may not require surgical intervention. Accepted for publication Jan 30, 1997. Children's Hospital Los Angeles and Department of Ophthalmology, University of Southern California. Inquiries to Talia Kolin, MD, Department of Ophthalmology, Chil dren's Hospital Los Angeles, 4650 Sunset Blvd, Los Angeles, CA 90027; fax: (213) 666-6283.
FIGURE 1. Slit-lamp photograph of persistent pupillary membrane in the right eye.
FIGURE 2. Slit-lamp photograph of persistent pupillary membrane in the left eye.
ERSISTENT PUPILLARY MEMBRANE IS AN INCOMPLETE
involution of the tunica vasculosa lentis. These membranes are attached to the iris collarette on one side while the other end is free floating, attached to 840
the lens, or attached to the iris on the opposite side. It is a congenital anomaly that is sporadic in most cases. These membranes do not usually impair visual acuity. However, large membranes that are presumed to result
AMERICAN JOURNAL OF OPHTHALMOLOGY
in amblyopia are often treated surgically. We report a child with extensive bilateral persistent pupillary membranes that have not been treated and that have not resulted in decreased vision or amblyopia. A 9-year-old girl with extensive bilateral hyperplastic pupillary membranes was initially examined as part of a routine eye examination. She had no history of ocular problems or complaints. She had a visual acuity of BE, 20/30, stereopsis of 50 seconds, orthophoria, and normal extraocular movements. Slit-lamp examination disclosed dense pupillary membranes in each eye (Figures 1 and 2). The remainder of the ophthalmic examination was normal. A clear view of the fundus was obtained in each eye. Persistence of an extensive pupillary membrane is uncommon. In those cases where a dense membrane exists, it is often difficult to assess in a nonverbal child whether this membrane is causing amblyopia. Many practitioners assume that a membrane similar to that in our patient is in itself a cause of occlusion amblyopia. In the ophthalmic literature, authors rec ommend surgical treatment of this condition before amblyopia develops. Before the refinement of anterior segment cataract surgery and the advent of viscoelastics, surgery to treat extensive pupillary membranes had been unsuccessful.1,2 As better techniques have developed, results have been more successful.3 Laser treatment of dense pupillary membranes is one such option,4,5 but it is not a procedure that can be performed in most facilities in children younger than age 6 years. Although surgeons may be less hesitant to operate on large membranes, especially in adults, this case demonstrates that any form of surgery may be unnecessary. Based on this patient, we have altered our treat ment of hyperplastic pupillary membranes. Mem branes should not be presumed to be causing amblyo pia; instead, the child should be observed until an age at which vision can be accurately assessed. Early surgical treatment may be associated with complica tions. Patching the good eye in a patient with a unilateral membrane may resolve the amblyopia with out resorting to surgery. Laser surgery can be per formed if needed in older patients. REFERENCES 1. Merin S, Crawford JS, Cardarelli J. Hyperplastic persistent pupillary membrane. A m J Ophthalmol 1973;72:717-719.
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2. Levy WJ. Congenital iris lesion. Br J Ophthalmol 1957;41: 120-123. 3. Cibis G W , Tripathi RC, Tripathi BJ. Surgical removal of congenital pupillary-iris-lens membrane. Ophthalmic Surg 1994;25:580-583. 4. Kumar H, Sakhuja N, Sachdev MS. Hyperplastic pupillary membrane and laser therapy. Ophthalmic Surg 1994;25: 189-190. 5. Yang W, Mao W. Nd:YAG laser treatment of congenital persistent pupillary membrane. Eye Sci 1991;7:120-124.
Streptococcal Toxic Shock Syndrome Complicating Preseptal Cellulitis Marcus A. Meyer, MD PURPOSE: Although substantial morbidity is un common in preseptal cellulitis, the incidence of severe infection resulting from group A strepto coccal infection is increasing. METHODS: A 62-year-old man was initially exam ined for preseptal cellulitis sustained after minor trauma to his brow. The patient rapidly experi enced shock and multisystem organ failure. In tensive medical therapy prevented circulatory collapse and death. RESULTS: A diagnosis of streptococcal toxic shock syndrome secondary to group A beta hemolytic streptococcal infection was made based on culture results and clinical course. CONCLUSIONS: The ophthalmologist plays an essential role in diagnosing this condition. Aggres sive and timely treatment are essential to prevent ing death.
TREPTOCOCCAL TOXIC SHOCK SYNDROME IS characterized by pain, high fever, confusion, desquamating rash, shock, and multiorgan failure. Di agnostic criteria include the isolation of group A streptococci from an infected site or blood, and two or more of the following conditions: renal impairment, coagulopathy, liver involvement, adult respiratory distress syndrome, a generalized erythematous rash with desquamation, or soft tissue necrosis.1 Treatment consists of intensive supportive therapy and institu-
Accepted for publication Dec 5, 1996. Department of Ophthalmology, Loyola University Chicago. Inquiries to Marcus A. Meyer, MD, 1139 S Wesley Ave, Oak Park, IL 60304; e-mail: [email protected]