FIGURE. Photograph taken from a videotape of sleeping child with upper eyelid eversion. Arrow indicates evert­ed left upper eyelid during sleep. Poor photographic resolution is the result of transfer from videotape.

teristic of the floppy eyelid syndrome (Figure). The left upper and lower eyelids were taped to close the palpebral fissure and to prevent ectropion during sleep. This treatment along with the application of ocular lubricants resolved all signs and symptoms of the floppy eyelid syndrome within several weeks.

Characteristic clinical associations in the floppy eyelid syndrome include punctate epithelial keratop-athy, keratoconus, and chronic papillary conjunctivi­tis, and affected individuals often have a history of sleeping on the affected side preferentially. Treatment options include taping the upper and lower eyelids to close the palpebral fissure and to prevent ectropion, as well as lubrication, eye shields, tarsorrhaphy, and horizontal eyelid-tightening surgery such as the lateral tarsal strip procedure. Histopathologic, electron mi­croscopic, and immunohistochemical studies of tissue removed during eyelid surgery to correct the floppy eyelid syndrome have shown a marked decrease in the amount of elastin fibers in the tarsal plates of affected patients.4

Theories regarding the origin of the floppy eyelid syndrome in obese patients have included systemic hypoventilation related to sleep apnea with reperfu-sion oxidation injury of the eyelid.5 Compression of the eyelids from sleeping on one side with subsequent eyelid ischemia has also been advanced as an expla­nation of this syndrome. This may possibly apply to

pediatric cases in which obesity and apnea are not primary contributing factors.

Our case demonstrates that the floppy eyelid syn­drome should be considered in the differential diag­nosis of chronic papillary conjunctivitis in patients at any age. In this pediatric case, video photography by the parents while the child was sleeping documented the eyelid ectropion and was a useful adjunct to more traditional diagnostic techniques.

REFERENCES

1. Culbertson WW, Ostler HB. The floppy eyelid syndrome. Am J Ophthalmol 1981;92:568-575.

2. Gerner EW, Hughes SM. Floppy eyelid with hyperglycemia. Am J Ophthalmol 1984;98:614-616.

3. Eiferman RA, Gossman MD, O'Neill K, Douglas CH. Floppy eyelid syndrome in a child. Am J Ophthalmol 1990;109: 356-357.

4. Netland PA, Sugrue SP, Albert DM, Shore JW. Histopatho­logic features of the floppy eyelid syndrome: involvement of tarsal elastin. Ophthalmology 1994;101:174-181.

5. Culbertson WW, Tseng SC. Corneal disorders in floppy eyelid syndrome. Cornea 1994;13:33-42.

Ocular Leech Infestation in a Child Turhan Alcelik, MD, Osman Cekic, MD, and Yuksel Totan, MD

PURPOSE: To describe a patient with manifesta­tions of ocular leech infestation. METHOD: Case report. RESULTS: The ocular foreign body was identified as a leech, Limnatis nilotica, by parasitologic examination. The leech was extracted, and the patient began using topical antibiotic and cyclople-gic agents. By the third day after extraction, the patient had no obvious symptoms or signs, except for a limited subconjunctival hemorrhage, and no epithelial defect on the cornea was observed. CONCLUSIONS: Ocular leech infestation should be considered in patients with a history of swim­ming in streams and lakes. Attention should also be given to ocular leech infestation in the differen­tial diagnosis of ocular trauma with iris prolapse.

Accepted for publication Feb 10, 1997. Eye Clinic of Social Security Company, Ankara Hospital. Inquiries to Osman Cekic, MD, 54 Basak Sokak, No. 7, 06660

Kucukesat-Ankara, Turkey; fax: +90-312-420 6964.

110 AMERICAN JOURNAL OF OPHTHALMOLOGY JULY 1997

A 7-YEAR-OLD BOY HAD PAIN, BURNING, ITCHING, foreign body sensation, and severe blepharo-

spasm of 1 day's duration in his left eye. The patient's history disclosed that irritation began after he had been swimming in a stream.

At the beginning of a standard ophthalmic exami­nation, the patient was agitated and unable to cooper­ate satisfactorily. The visual acuity of the affected eye could not be measured accurately because of severe blepharospasm. The upper and lower eyelids appeared to be edematous and hyperemic. After instilling topical anesthetic drops, we were able to open die patient's eyelids, disclosing secretion and conjunctival hyperemia. Initial biomicroscopy of the affected eye showed a mass of tissue resembling iris prolapse (Figure 1, top). Further retraction of the upper eyelid disclosed that the tissue mass extended from the superior peripheral cornea to the adjacent conjuncti­va, with surrounding subconjunctival hemorrhage. There was also superficial and deep conjunctival hyperemia (Figure 1, bottom). The mass was similar to the iris in color; however, it was mobile.

In a detailed examination, only the section of the cornea beneath the mass was slightly edematous. However, anterior chamber depth as well as the size, position, and shape of the pupil were within normal limits. No keratic precipitate or cell in the anterior chamber was detected. The lens and vitreous were clear. Fundus examination disclosed no pathologic finding. Intraocular pressure of the affected eye was estimated digitally to be within normal ranges. In the right eye, visual acuity was 20/20, and examination disclosed normal anterior and posterior segment structures. The patient had no pertinent systemic symptoms or signs. Laboratory values showed normal blood cell count and biochemistry.

After instilling topical anesthetic drops, we used a forceps to extract the living foreign body from the cornea and adjacent bulbar conjunctiva. A localized subconjunctival hemorrhage and superficial corneal epithelial defect appeared after the extraction (Figure 2). We applied topical antibiotic drops and ointment and a cycloplegic agent; we then patched the injured eye. By the third day after extraction, there were no obvious symptoms or signs, except a limited subcon­junctival hemorrhage, and no epithelial defect on the cornea was observed. Measured with a pinhole, visual acuity of the affected eye was 20/20. The parasitology

FIGURE 1. (Top) The initial appearance of the leech, resembling iris prolapse. (Bottom) The leech extending from upper peripheral cornea to adjacent conjunctiva, with surrounding subconjunctival hemorrhage.

FIGURE 2. The localized subconjunctival hemorrhage and superficial corneal epithelial defect after the extrac­tion of the leech.

VOL.124, No. 1 BRIEF REPORTS 111

department identified the formalin-fixed specimen as a leech, Limnatis nilotica, based on the following characteristics: 1.2 cm in length and 0.4 cm in width, no auricle on the posterior segment, no spots but 34 somites, five pairs of eye, and numerous teeth.

Although nasal and pharyngeal leech infestations have been reported before,1,z this is the first case of ocular leech infestation in the literature. Leeches can adhere to the surface of the oropharynx, nasophar­ynx, and nasal fossa, and patients affected as such may have profuse nasal bleeding and hemoptysis.1 The contemporary uses of medicinal leeches have includ­ed the evacuation of periorbital hematoma.3

Ocular leech infestation should be considered in the differential diagnosis of ocular foreign bodies and penetrating ocular trauma with iris prolapse.

REFERENCES

1. Golz A, Zohar S, Avraham S, Joachims HZ, Danino J, Merzbach D. Epistaxis caused by leeches. Harefuah 1989;117: 141-143.

2. Makiya K, Tsukamoto M, Horio M, Kuroda Y. A case report of nasal infestation by the leech, Dinobdella ferox. Sangyo Ika Daigaku Zasshi 1982;10:203-209.

3. Bunker TD. The contemporary use of the medicinal leech. Injury 1981;12:430-432.

Dominant Inheritance of Optic Pits S. Tonya Stefko, BS, Peter Campochiaro, MD, Peiyi Wang, BS, Yingying Li, MD, Danping Zhu, MD, and Elias I. Traboulsi, MD

PURPOSE: To report the familial occurrence of optic pits and to screen the candidate PAX2 gene for mutations in this family. METHODS: Clinical family study. Standard muta­tion analysis of the PAX2 exons. RESULTS: Unilateral optic pits were present in three generations of one family and were inherited in an autosomal dominant fashion. No mutations in the PAX2 gene, responsible for the renal-optic coloboma syndrome, were found. CONCLUSION: Unilateral optic pits may be inher­ited in an autosomal dominant fashion and not in association with mutation in the PAX2 gene.

C ONGENITAL PITS OF THE OPTIC NERVE HEAD ARE

isolated, generally nonfamilial unilateral malfor­mations. They have a characteristic appearance and are complicated by serous macular detachment in up to 50% of patients.1 They are rarely familial, and we are aware of only two reports of affected parent-child pairs.2'3 We examined a woman, her son, and her grandson, all with unilateral optic pits (Figure 1).

The family was ascertained through the examina­tion of the grandchild. He developed a serous macular detachment in the right eye at the age of 8 years and was found to have an optic pit (Figure 2, top). He had a congenital red/green color deficiency. His visual acuity fluctuated during the next 2 years between RE, 20/30 and 20/60. Subsequently, it dropped to 20/100, and he underwent vitrectomy, gas-fluid exchange, and endolaser photocoagulation to the temporal edge of the disk. Visual acuity improved to RE, 20/30 during the next year.

The patient's father had experienced episodes of fluctuating vision during his adolescence. His present visual acuity was 20/20 in each eye. There was a pit of his left optic disk, with ophthalmoscopic evidence of previous serous macular detachment (Figure 2, mid­dle). Similarly, the grandmother was found to have a small temporal optic pit of her right eye (Figure 2, bottom) and a visual acuity of RE, 20/20. The patient's two sisters were examined and were found not to have optic pits.

Because of the recent report of mutations in the PAX2 gene in two families with optic nerve coloboma and renal abnormalities,4,5 we analyzed this paired box-containing developmental gene located at 10q24-q25 for mutations in this family according to the methodology published by Sanyanusin and asso­ciates4,5 (exons in coding region) and personally communicated to us by Dr Michael Eccles (exons in noncoding region) (MR Eccles, PhD, written com­munication, Nov 1996). No mutations were found.

Optic pits may be inherited in an autosomal dominant fashion, and in this and in previous reports,2,3 they have occurred only in one eye of affected family members. Although mutations in the

Accepted for publication Feb 24, 1997. The Johns Hopkins Center for Hereditary Eye Diseases, The Wilmer

Ophthalmological Institute. Inquiries to Elias I. Traboulsi, MD, Maumenee 517, 600 N Wolfe St,

Baltimore, MD 21287; fax: (410) 614-4363.

112 AMERICAN JOURNAL OF OPHTHALMOLOGY JULY 1997