Ocular Cytopathology

An atlas that features the cytologic findings of the normal features and diseases of the eye.

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Friday, September 30, 2005

Ch 7. Eales Disease of the Retina

EALES’ DISEASE

Eales’ disease was initially described in young males with vitreous hemorrhage and abnormal retinal veins.[59] Now it is clinically defined by an obliterative vasculopathy involving both venules and arterioles (Figure 7-9).[60] In the late stages, ischemia leads to neovascularization with resulting vitreous hemorrhage, retinal detachment, and secondary glaucoma.[61][62] Specimens are obtained when vitrectomy is done to remove persistent vitreous hemorrhage or extraretinal fibrous tissue.[63] Cytologic specimens may show vitreous hemorrhage (hemoglobin spherulosis) and, occasionally, fibrous tissue (Figure 7-10).
Other conditions that produce neovascularization and vitreous hemorrhage include branch retinal vein occlusion,[64] sickle cell retinopathy,[65] carotid and aortic arch occlusive syndromes,[66] and hyperviscosity syndromes.[67]
References:
59. Eales H. Cases of retinal hemorrhage associated with epistaxis and constipation. Birm Med Rev 1880;9:262.
60. Elliot AJ. Thirty-year observation of patients with Eales' disease. Am J Ophthalmol 1975;80:404-408.
61. Renie WA, Murphy RP, Anderson KC, Lippman SM, McKusick VA, et al. The evaluation of patients with Eales' disease. Albrecht Von Graefes Arch Klin Exp Ophthalmol 1975;194:73-85.
62. Spitznas M, Meryer-Schwickerath GT, Staphan B. The clinical picture of Eales' disease. Albrecht Von Graefes Arch Klin Exp Ophthalmol 1975;194:73-85.
63. Gieser SC, Murphy RP. Eales' disease. In: Ryan SJ, Schachat AP, Murphy RP, Patz A, eds. Retina. St. Louis: C.V. Mosby, 1989;2:535-540.
64. Heyreh SS, Rojas P, Podhajsky P, Montague P, Woolson RF. Ocular neovascularization with retinal vein occlusion. Ophthalmology 1983;20:488-506.
65. Goldberg MF. Classifcation and pathogenesis of proliferative sickle retinopathy. Am J Ophthalmol 1971;71:649-665.
66. Kahn M, Green WR, Knox DL, MIller NR. Ocular features of carotid occlusive disease. Retina 1986;6:239-252.
67. Ring CP, Pearson TC, Sanders MD, Wetherly Mein G. Viscosity and retinal vein thrombosis. Br J Ophthalmol 1967;60:397-410.



Diabetic Retinopathy, Coats Disease, Proliferative Vitreoretinopathy

COATS’ DISEASE

Coats’ disease is usually unilateral and is characterized by exudative retinal detachment in young males.[19][20][21] Telangiectatic blood vessels have been identified in this disorder and presumably are the basis for the retinal exudates and exudative detachment of the retina (Figure 7-3).[22][23] Coats’ disease may produce leukocoria in children and can be confused clinically with retinoblastoma. In such cases, a fine needle aspiration may be obtained to differentiate these two entities. In addition, a vitrectomy may be employed to repair the retinal detachment.[24][25][26] In either case, the specimens are extremely hypocellular with occasional macrophages containing cytoplasmic vacuoles (Figure 7-4).[27] Histologically, there is massive subretinal exudates and retinal detachment. Telangiectasis of the retinal blood vessels or the extraretinal blood vessels can be identified (Figure 7-5).

DIABETIC RETINOPATHY

Diabetic retinopathy is the single most common source of intraocular washing specimens processed by our cytology laboratory. Retinopathy occurs in about 70% of patients who have had diabetes mellitus beyond 20 years. Diabetic retinopathy manifests as a microangiopathy with thickening of vascular basement membrane, loss of endothelium, and degeneration of capillary pericytes.[28][29][30][31][32] In the early stages, venous dilatation, capillary microaneurysms, and exudates are observed.[33][34] Vascular disease leads to ischemia of the retina and neovascularization is stimulated (proliferative diabetic retinopathy) (Figure 7-6).[35][36] Vitrectomy may be performed in this disease for several reasons, including vitreous hemorrhage secondary to neovascularization and tractional retinal detachment with removal of fibrovascular membrane.[37][38][39]
Neovascularization is identified in vitrectomy specimens as well-defined blood vessels lined by a single layer of endothelium (Figure 7-7).

PROLIFERATIVE VITREORETINPATHY

The leading cause of failure in retinal detachment surgery is proliferative vitreoretinopathy (PVR).[40][41][42][43] It is characterized by a proliferation of cellular membranes on both sides of the detached retina and in the vitreous cavity.[44] Fibrovascular proliferation that extends anterior to the posterior border of the vitreous base has been termed anterior PVR.[45] Traction induced from the membranes on the posterior lens surface, ciliary body, and iris may produce a peripheral retinal detachment.[46] Epiretinal membranes are composed of retinal pigment epithelial cells, glial cells, fibrocytes, and macrophages.[47][48][49][50][51][52][53][54][55][56] Surgically removed epiretinal membranes may be sent for cytologic examination. Cell buttons or cytospin preparations reveal a thin fragment composed of spindle cells and oval cells, some of which may contain pigment (Figure 7-8).
Epiretinal membranes composed mainly of spindle cells have been associated with photocoagulation, trauma, and inflammatory disease.[57] However, most simple epiretinal membranes are idiopathic.[58]
References:
19. Coats G. Royal London Ophthal Hosp Rep 1908;17:440-525.
20. Fox KR. Metabol Pediatr Syst Ophthalmol 1980;4:121-124.
21. Reese AB. Am J Ophthalmol 1956;42:1-8.
22. Chang M, McLean IW, Merritt JC. J Pediatr Opthalmol Strabismus 1984;21:163-168.
23. Egbert PR, Chan CC, Winter FC. J Pediatr Ophthalmol 1977;13:336-339.
24. Jaffe MS, Shields JA, Canny CLB, Eagle RC, Fry RL. Ann Ophthalmol 1977;9:863-868.
25. Pe'er J. Am J Opthalmsol 1988;106:742-743.
26. Laqua H, Wessing A. Ophthalmology 1983;90:1284-1291.
27. Haik BG, Koizumi J, Smith ME, Ellsworth, RM. Am J Opthalmol 1985;100:327-328.
28. Robison WG Jr. Kador PF, Kinoshita JH. Science 1983;221:1177.
29. Kalebic T, Garbisa S, Glaser B, Liotta LA.Science 1983;221:281.
30. Kuwabara T, Cogan DG. Arch Ophthalmol 1963;69:492-502.
31. Toussaint D, Dustin P. Arch Ophthalmol 1963;70:96-108.
32. Yanoff M. N Engl J Med 1966;274:1344-1349.
33. De Venecia G, Davis M, Engerman R. Arch Ophthalmol 1976;94:1766-1773.
34. Addison DJ, Garner A, Ashton N. Br Med J 1970;1:264-266.
35. Niki T, Muraoka K, Shimizu K. Ophthalmology 1984;91:1440.
36. Miller H, Miller B, Zonis S, Nir I. Invest Ophthalmol Vis Sci 1984;25:1338-1342.
37. Thompson JT, de Bustros S, Michels RG, Rice TA. Arch Ophthalmol 1987;105:503-507.
38. Thompson JT, de Buustros Michels RG, Rice TA. Arch Ophthalmol 1987; 105:191-195.
39. Blankenship GW. St Louis: C.V. Mosby, 1989;3:515-539.
40. The Retinal Society Terminology Committee. Ophthalmology 1983;90:121-125.
41. Claes C, Freeman HM, Tolentino FI. New York: Springer-Verlag, 1988:3-11.
42. Lewis H, Aaberg TM, Abrams GW. Am J Ophthalmol 1991;111:8-14.
43. Schwartz D, De la Cruz ZC, Green WR, Michels RG. Retina 1988;8:275-281.
44. Glaser BM. Pathobiology of PVR. New York: Springer-Verlag, 1988:12-21.
45. Lewis H, Aaberg T. Am J Ophthalmol 1988; 105:277.
46. Lewis H, Abrams GW, Foos RY. Am J Ophthalmol 1987;104:614-618.
47. Machemer R, Laqua H. Am J Ophthalmol 1975;80:1-23.
48. Clarkson JG, Green WR, Massoff D. Am J Ophthalmol 1977;84:1-17.
49. Daicker B, Guggenheim R. Albrecht Von Graefes Arch Klin Exp Ophthalmol 1979;210:109-110
50. Van Horn DL, Aaberg TM, Machemer R. Am J Ophthalmol 1977;84:383-393.
51. Kampik A, Kenyon KR, Michels RG, Green WR, de Cruz ZC, Epiretinal and vitreous membranes: comparative study of 56 cases. Arch Ophthalmol 1981;198199:1445-1454.
52. Kampik A, Green WR, Michels Rg, Nase PK. Ultrastructure of progressive idiopathic epiretinal membrane removed by vitreous surgery. Am J Ophthalmol 1980:90:797-809.
53. Hiscott PS, Grierson I, McLeod D. Natural history of fibrocellular epiretinal membranes: a quanative, autoradiographic and immunohistochemical study. Br J Ophthalmol 1985;69:810-823.
54. Michels RG. A clinical and hisopathical study of epiretinal membranes affecting the macula and removed bu vitreous surgery. Trans Am Ophthalmol Soc 1982;80:580-656.
55. Foos RY. Spectrum of nonvasular proliferative extraretinopathies. In: Nicholson DH, ed. Ocular pathology update. New York: Masson Publishing, 1980:107-114.
56. Foos RY. Nonvascular proliferative extraretinopathies. Am J Ophthalmol1978;86:723-725.
57. Kampik A, Green WR, Michels RG, Rice TA. Epiretinale membranen nack photokoagulation (postkoagulative maculopathie). Ber Dtsch Ophthalmol Ges 1981;78:593-598.
58. Roth AM, Foos RY. Surface wrinking retinopath in eyes enucleated at autotopsy. Trans AM Acad Ophthalmol Otolaryngol 1971;75:1047-1058.



CHAPTER 7 Retinopathy of Prematurity

Abnormalities of the Retina

Our goal in this chapter is to introduce those retinal diseases that are most commonly encountered in cytology specimens. The diagnosis of many of these lesions by cytologic techniques alone can be difficult and thorough familiarity with the tissue lesion can be very helpful.
The ocular cytologist is likely to encounter specimens from only a few retinal diseases on a routine basis. Intraocular washings from patients with diabetic retinopathy and proliferative vitreoretinopathy account for most of the specimens. Because the diagnosis is often apparent from clinical examination, some argue that it is superfluous to send the intraocular washings for pathologic examination. Indeed, only 15% of intraocular washings are diagnostic of specific diseases.[1] However, the need to exclude clinically unsuspected infectious and neoplastic disorders justifies routine processing of vitrectomy specimens. Examination of intraocular washings sometimes reveals retinal fragments. It is often difficult to diagnose specific diseases from retinal fragments seen in cytologic preparations. Other accompanying fragments usually provide clues to the diagnosis. Notable exceptions in which diseases are diagnosed by retinal biopsies include infectious retinitis and retinoblastoma. These entities are discussed separately in Chapters 8 and 9, respectively.

RETINOPATHY OF PREMATURITY

Previously called retrolental fibroplasias,[2] retinopathy of prematurity is a disease of the premature infant.[3] It is usually, but not always, associated with exposure to high concentration of oxygen.[4][5][6][7] The natural history and pathogensis of these diseases is discussed in detail elsewhere.[8][9][10][11] In brief, retinopathy of prematurity develops at the border of the developing retinal vasculature.[12][13] Presumably, ischemia leads to proliferation of the primitive microvasculature, which in turn may lead to tractional retinal detachment (Figure 7-1).[14][15]
Vitrectomies are preformed in the late stages to remove the vitreous and fibrovascular tissue in order to repair the retinal detachment.[16][17] When the retina is detached, the visual prognosis is poor.[18] In cytologic preparations, fibrous tissue, lens fragments (lensectomy), pigment-laden macrophages, and vitreous hemorrhage can be observed (Figure 7-2). These findings are not specific for retinopathy of prematurity.
References:
1. Green WR. Ophthalmology 1984;91:726-749.
2. Foos RY. Albrecht Von Graefes Arch Klin Exp Ophthalmol 1975;195:87-100.
3. Keith CG, Kitchen WH. Med J Aust 1984;141:225-227.
4. Patz A. Am J Ophthalmol 1985;100:164-168.
5. Kushner BJ, Gloeckner E. Am J Ophthalmol 1984;27:148-163.
6. Shohat M, Reisner SH, Krikler R, Nissonkorn I, Yassur Y, et al. Pediatrics 1983;72:159-163.
7. Karlsberg RC, Green WR, Patz A. Arch Ophthalmol 1973:89:122-123.
8. Flynn JT, Bancalari E, Bachynski BN, Buckley EB, Bawd R, et al. Ophthalmology 1987;94:620-629.
9. Prendiville A, Schulenberg WE. Arch Dis Child 1988;63:522-527.
10. Silverman WA, Flynn JT. Boston: Blackwell Scientific, 1985.
11. McPherson AR, Hittner HM, Kretzer FL. Toronto: B.C. Decker, 1986.
12. Foos RY. Retina 1987;7:260-276.
13. Kushner BJ, Essner D, Cohen IJ, Flynn JT. Arch Ophthalmol 1977;95:29-38.
14. Campbell FW. Trans Ophthalmol Soc UK 1951;71:287-300.
15. Quinn GE, Schaffer DB, Johnson L. Am J Ophthalmol 1982;94:744-749.
16. Lightfoot D, Irvine AR. Am J Ophthalmol 1982;94:305-312.
17. Schepens CL. Am J Ophthalmol 1981;91:143-171.
18. Jabbour NM, Eller AE, Hirose T, Schepens CL, Liberfarb R, et al. Ophthalmology 1987;94:1640.


Thursday, September 29, 2005

Amyloidosis, Silicone Vitreoretinopathy, pg2

AMYLOIDOSIS

Vitreous amyloidosis is usually associated with primary familial amyloidosis. It is important to recognize vitreous amyloidosis because it may be the presenting sign or symptom of both systemic and ocular lesions, including proptosis, ocular palsies, internal ophthalmoplegia, neuroparalytic keratitis, glaucoma, and conjunctival involvement. [18, 19, 20, 21, 22, 23, 24]
Amyloidosis in the vitreous is causally linked with retinal blood vessel involvement. Vitreous amyloid may be dense enough to obscure vision or may be misinterpreted clinically as vitreous hemorrhage. [25] Biomicroscopically, the opacities may appear yellow-white and have a membranous veil-like quality (Figure 6-7). Some authors have described a central white dot associated with vertically oriented yellow strands. [26]
Vitrectomy may be done as a diagnostic or therapeutic maneuver. [27, 28, 29, 30] Intraocular washings reveal amorphous birefringent deposits that are enhanced with Congo red stain (Figure 6-8). Red-green dichroism may be observed in specimens stained with Congo red and illuminated with polarized light (Figure 6-9). Amyloid fluoresces with thioflavin T stain. It has been demonstrated that vitreous amyloid reacts immunocytochemically with antibody to prealbumin. [31] Familial amyloidosis of the neuropathic type has been associated with homozygosity for the transthyretin methionine-30 gene. [32]

SILICONE VITREORETINOPATHY

Silicone oil is used retinal detachment surgery as a means to tamponade retinal breaks and reattach the retina. [33, 34, 35] It is often reserved for cases of recurrent retinal detachments and advanced proliferative vitreoretinopathy. [36] There is experimental and clinical evidence to suggest that silicone oil may stimulate fibrous proliferation and recurrent membrane formation. [37, 38, 39, 40] Histologic studies have demonstrated glial or pigment epithelial tissue containing vacuoles as well as extracellular clear spaces. [41] Cytologic preparations show intracellular vacuoles that presumably represent silicone oil engulfed by glial cells and macrophages (Figure 6-10).

HEALON-LADEN MACROPHAGES

The differential diagnosis of clear vacuoles within macrophages includes residual healon (hyaluronic acid polymer). This viscoelastic substance is used mainly during cataract surgery to keep the ocular chambers formed so instruments glide smoothly through incisions and the corneal endothelium is protected from damage. Cytologic specimens show macrophages with cytoplasmic clear spaces (Figure 6-11). A proliferative reaction has not been reported with healon.

REFERENCES:
18. Lieberman TW, Ferry AP. Trans Am Ophthalmol Soc 1974;72:302-325
19. Kaufman HE. Arch Ophthalmol 1958;60:1036-2043
20. Crawford JB. Arch Ophthalmol 1967;78:214-216
21. Wong VG, McFarlin DE. Arch Opththalmol 1967;78:208-213
22. Legrand J. Guenel J, Dubigeon P. Bull Soc Ophtalmol Fr 1968;68:13-20
23. Hamburg A. Ophthalmologica 1971;162:173-177
24. Franceschetti AT, Rabinowicz T. J Genet Hum 1969;17:349-366
25. Schwartz MF, Green WR, Michels RG, Kincaid MC, Fogle J. Ophthalmology 1982;89:394-401
26. Mieler WF, Williams DF, Levin M. Arch Ophthalmol 1988;106:881-883
27. Paton D, Duke JR. AJO 1966;51:736-747
28. Kasner D, Miller GR, Taylor WH, Sever RJ, Norton EW, et al Trans Am Acad Ophthalmol Otolaryngol 1968;72:410-418
29. Matsui M, Tashiro T, Asai Y. Acta Soc Ophthalmol Jpn 1976;80:142-146
30. Irvine AR. Char DH. AJO 1976;82:705-708
31. Doft BH, Rubinow A, Cohen AS. AJO 1984;97:296-300
32. Sandgren O, Holmgrem G, Lundgren E. Arch Ophthalmol 1990;108:1584-1586
33. Cibis PA, Becker B, Okun E, Canaan S. Arch Ophthalmol 1962;68:590-599
34. Grey RHB, Leaver PK. BF J Ophthalmol 1979;92:1029-1034
35. McCuen BW II, Landers MB III, Machemer R. Ophthalmology 1985;92:1029-1034
36. Cox MS, Trese MT, Murphy PL. Ophthalmology 1986;93:646-650
37. Fastenberg DM, Diddie KR, Delmage JM, Dorey K. AJO 1983;95:663-667
38. Gonvers M, ThresherR. Graefes Arch Clin Exp Ophthalmol 1983;221:46-53
39. Watzke RC. Arch Ophthalmol 1967;77:185-196
40. Cockerham WD, Schepens CL, Freeman HM. Arch Ophthalmol 1970;83:704-712
41. Lewis H, Burke JM, Abrams GW, Aaberg TM. Ophthalmology 1988; 95:583-591




CHAPTER 6 Vitreous Abnormalities page 1

CHAPTER 6 Abnormalities of the Vitreous Body

Most abnormalities of the vitreous body (vitreous) are too subtle to be diagnosed by intraocular washings alone. These subtle changes are diagnosed by careful biomicroscopic examination in the living patient or with the dissecting microscope in the enucleated specimen. However, there are a few important conditions, such as amyloid, silicone retinopathy, and asteroid hyalosis, that are evident by examination of extracted vitreous. Other conditions, such as persistent hyperplastic primary vitreous, are considered in the clinical diagnosis of malignant tumors in children and it is important to be aware of their existence. Vitreous hemorrhage and hemoglobin spherulosis are presented in Chapter 5.

PERSISTENT HYPERPLASTIC PRIMARY VITREOUS

Persistent hyperplastic primary vitreous (PHPV) is a congenital condition most commonly unilateral in which there is persistent hyaloid vasculature and mesenchymal tissue from the embryonic primary vitreous in a microphthalmic eye. [1, 2, 3] Fibrovascular tissue and mesenchymal tissue are attached laterally to elongated and centrally dislocated ciliary processes (Figure 6-1 and 6-2). The lens-iris diaphragm may be anteriorly displaced and produce secondary angle-closure glaucoma. Cartilage, mature adipose tissue, and smooth muscle may arise from primitive mesenchymal tissue behind the lens. [4, 5, 6] There is frequently an accompanying total exudative retinal detachment (Figure 6-1). Clinically, the patient usually has a white papillary reflex (leukocria), poor vision, and a small eye. PHPV can be confused with retinoblastoma, although existence of leukocoria at birth and microphthalmia is highly suggestive of PHPV. If retinoblastoma is a series consideration in the differential diagnosis or if surgical repair is considered for PHPV, preoperative fine needle aspiration or intraocular washing may be used. Smears show spindle cells and retinal tissue (Figure 6-3). Unlike retinoblastoma, the cells of PHPV are usually more cohesive and do not exhibit extensive necrosis.

ASTEROID HYALOSIS

Asteroid hyalosis is a disorder in which white-yellow smooth refractile spheres are suspended in the collagenous framework of the vitreous body. It is often unilateral, but can be bilateral. It is more common in older people. [7] The opacities are composed of complex lipids, calcium, and phosphorous. [8, 9, 10] Histochemically, the matrix of the opacities stain with periodic acid-Schiff, alcian blue, Sudan black B, and oil red O. [11] clinically asteroid hyalosis is often asymptomatic with good visual acuity. However, it may be very dense and it may obscure vision. [12, 13] In addition, the poor funduscopic view occasionally prevents adequate laser photocoagulation in patients with concomitant retinopathy (Figure 6-4). Vitrectomy may be indicated to improve vision or to improve the view of the fundus for the surgeon. [14] Cytologic specimens reveal amorphous round bodies that are birefringent in polarized light (Figures 6-5 and 6-6). There may be an associated foreign-body reaction. [10]
The cause of asteroid hyalosis is not known. Even though lipid is present in the yellow particles, there is no clear association with diabetes and hypercholesterolemia. [15, 16, 17]
References:
1. Reese AB. Arch Ophthalmol 1949;41:527-549.
2. Reese AB. AJO 1955;40:317-331.
3. Haddad R, Font, RL, Reeser F. Surv Ophthalmol 1978;23:123
4. Font RL, Yanoff M, Zimmerman LE. Arch Ophthalmol 1969;82:43-50
5. Manschot WA. Arch Ophthalmol 1958;59:188-203
6. Reese AB, Payne F. AJO 1964;29:1-19
7. Rutherford CW. Arch Ophthalmol 1933;9:106
8. Verhoeff FH. AJO 1921;4:155-160
9. March W, Shock D, O' Grady R. Invest Ophthalmol 1974;13:701705
10. Miller H, Miller B, Rabinowitz H, et al. Invest Ophthalmol Vis Sci 1983;24:133-136
11. Rodman HI, Johnson FB, Zimmerman LE. Arch Ophthalmol 1961;66:552-563
12. Engel HM, Green WR, Michels RG, Rice TA, Erozan YS, et al. Retina 1981;1:121-149
13. Renaldo DP. Retina 1981;1:252-254
14. Lambrou FH, Sternberg P, Meredith TA, Mines J, Fine SL. Ophthalmic Surg 1989;20:100-102
15. Smith JL. JAMA 1958;168:891-893
16. Hatfield RE, Gastineau CF, Rucker CW. Mayo Clin Proc 1962;37:513-514
17. Luxenberg MN, Sime D. AJO 1969;67:406-413






Wednesday, September 28, 2005

Chapter-5-page4-References-CiliaryBody

14. Bonamour MM, Bonnet JC, Jambon M. Leiomyome du corps ciliaire; quelques considerations a propos du diagnostic et du traitement des tumeur benignes de l’iris et du corps ciliaire. Bull Soc Ophtalmol Fr 1957;7-8:482.
15. Calmettes L, Deodati F, Bec P. Leiomyome du corps ciliare. Bull Soc Ophtalmol Fr 1961;74:158-168.
16. Allen RA. Leiomyoma of ciliary body. Case presented at the Verhoeff Society, Washington, D.C., April 24-27, 1967.
17. Meyer SL, Fine BS, Front RL, Zimmerman LE. Leiomyoma of the ciliary body. Electron microscopic verification. Am J Ophthalmol 1968;66:1061-1068.
18. Calhoun FP Jr. Leiomyoma of the ciliary body. Case presented at the Verhoeff Society, Washington, D.C., April 26-29, 1976.
19. Jakobiec FA, Font RL, Tso MOM, Zimmerman LE. Mesectodermal leiomyoma of the ciliary body. A tumor of presumed neural crest origin. Cancer 1977;3 9:2102-2113.
20. Jakobiec FA, Iwamoto T. Mesectodermal leiomyoma of the ciliary body associated with a nevus. Arch Ophthalmol 1978;96:692-695.
21. Zimmerman LE. Melanocytes, melanocytic nevi, melanocytomas. Invest Ophthalmol 1965;4:11-40.
22. Reidy JJ, Apple DJ, Steinmetz RL, et al. Melanocytoma nomenclature, pathogensis, natural history and treatment. Surv Ophthalmol 1985;29:319-327.
23. Frangieh GT, El Baba F, Traboulsi El, et al. Melanocytoma of the ciliary body: presentation of four cases and review of nineteen reports. Surv Ophthalmol 1985;29:328-334.
24. Streeten BF, McGraw JL. Tumor of the ciliary pigment epithelium. Am J Ophthalmol 1972;74:420-429.
25. Wilensky JT, Holland MG. A pigmented tumor of the ciliary body. Arch Ophthalmol 1974;92:219-220.
26. Chang M, Shields JA, Wachtel DL. Adenoma of the pigment epithelium of the ciliary body simulating a malignant melanoma. Am J Ophthalmol 1979;88:40-44.
27. Anderson SR. Medulloepithelioma of the retina. In: Zimmerman LE, ed. Tumors of the eye and adnexa. Int Ophthalmol Clin 1962;2:483-506.
28. Leib WE, Shields JA, Eagle RC, Kwa D, Shields CL Cystic adenoma of the pigmented ciliary epithelium. Ophthalmol 1990;97:1489-1493.
29. Char DH, Miller TR, Crawford JB. Cytopathologic diagnosis of benign lesions simulating choroidal melanomas. Am J Ophthalmol 1991;112:70-75.
30. Jensen OA. Malignant melanoma of the human uvea. Acta Ophthalmol (Suppl.) 1963;75:17-215.
31. Raivio I. Uveal melanomas in Finland; an epidemiological, clinical, histological and prognostic study. Acta Ophthalmol (Suppl.) 1977;133:1-64.
32. Apt L. Uveal melanomas in children and adolescents. Int Ophthalmol Clin 1963;2:403-410.
33. Holland G. Clinical features and pathology of pigment tumours of the iris. Klin Monatsbl Augenheikd 1967;150:350-370.
34. Rones B, Zimmerman LE. The prognosis of primary tumors of the iris treated by iridectomy. Arch Ophthalmol 1958;60:193-205.
35. Shields JA, Sandborn GE, Augsburger JJ. The differential diagnosis of malignant melanoma of the iris. A clinical study of 200 patients. Ophthalmol 1983;90:716-720.
36. Callender GR. Malignant melanotic tumors of the eye. A study of histologic types in 111 cases. Trans Am Acad Ophthalmol Otolaryngol 1931;36:131.
37. Jakobiec FA, Silbert G. Are most iris “melanomas” really nevi? Arch Ophthalmol 1981;99:2117-2132.
38. Arentsen JJ, Green WR. Melanoma of the iris: report of 72 cases treated surgically. Ophthalmic Surg 1975;6:23-37.
39. Ashton N. Primary tumours of the iris. BR J Ophthalmol 1964;48:650-668.
40. Char DH, Crawford JB, Gonzales, Miller T. Iris melanoma with increased intraocular pressure. Differentiation of focal solitary tumors from diffuse or multiple tumors. Arch Ophthalmol 1989;107:548-551

chapter-5-page3-Iris, Ciliary Body, Melanoma

IRIS AND CILIARY BODY MELANOMA

Melanomas in the eye most commonly occur in the choroids (see Chapter 9). However, about 3% to 16% (41% in children) of ocular melanomas arise in the iris and 9% to 10% arise in the ciliary body. [30, 31, 32, 33] Clinically, iris melanomas are highly vascular, pigmented lesions that usually occur inferiorly in the iris. [34, 35] The Callender classification of uveal melanomas as spindle or epithelioid does not apply to iris melanomas. [36, 37, 38] Iris melanomas have a much better prognosis than their ciliary body and choroidal counterparts. [39] Occasionally, malignant melanomas extend circumferentially about the ciliary body, yet clinically only a focus iris lesion is present (Figure 5-16). Determination of cell type in these cases may be helpful to document the presence of nucleoli suggesting a more atypical type of melanoma (Figure 5-17). Fine needle may be quite helpful in determining the presence of a ring melanoma of the ciliary body if the aspirate is performed away from the apparent lesion (Figure 5-18 and 5-19). Fine needle aspiration has been used to diagnosis iris masses and, specifically, to help determine if a pigmented lesion in the iris or ciliary body is focal, multiple, or diffuse. [40] However, on cytologic criteria alone, it is not possible to determine the original site of melanomas.

REFERENCE


30. Jensen OA. Malignant melanoma of the human uvea. Acta Ophthalmol (Suppl.) 1963;75:17-215.
31. Raivio I. Uveal melanomas in Finland; an epidemiological, clinical, histological and prognostic study. Acta Ophthalmol (Suppl.) 1977;133:1-64.
32. Apt L. Uveal melanomas in children and adolescents. Int Ophthalmol Clin 1963;2:403-410.
33. Holland G. Clinical features and pathology of pigment tumours of the iris. Klin Monatsbl Augenheikd 1967;150:350-370.
34. Rones B, Zimmerman LE. The prognosis of primary tumors of the iris treated by iridectomy. Arch Ophthalmol 1958;60:193-205.
35. Shields JA, Sanborn GE, Augsburger JJ. The differential diagnosis of malignant melanoma of the iris. A clinical study of 200 patients. Ophthalmol 1983;90:716-720.
36. Callender GR. Malignant melanotic tumors of the eye. A study of histologic types in 111 cases. Trans Am Acad Ophthalmol Otolaryngol 1931;36:131.
37. Jakobiec FA, Silbert G. Are most iris “melanomas” really nevi? Arch Ophthalmol 1981;99:2117-2132.
38. Arentsen JJ, Green WR. Melanoma of the iris: report of 72 cases treated surgically. Ophthalmic Surg 1975;6:23-37.
39. Ashton N. Primary tumours of the iris. BR J Ophthalmol 1964;48:650-668.
40. Char DH, Crawford JB, Gonzales, Miller T. Iris melanoma with increased intraocular pressure. Differentiation of focal solitary tumors from diffuse or multiple tumors. Arch Ophthalmol 1989;107:548-551


Chapter-5-page2-Coronal Adenoma, Leiomyoma

CORONAL ADENOMA
The coronal adenoma, also called benign adenoma, Fuch’s adenoma, Fuch’s epithelioma, and epithelial hyperplasia, is the most common intraocular tumor. [6, 7] These adenomas originate from the nonpigmented epithelium of the pars plicata (the coronal processes) (Figure 5-6). They occur more commonly in older individuals. [8] Histologic sections show nonpigmented ciliary epithelium embedded in a matrix of basement membrane material (Figure 5-7). Rarely, these tumors are clinically misdiagnosed as melanoma because they indent the iris and mimic a pigmented lesion. [9, 10]Aspiration biopsy will distinguish melanoma from coronal adenoma. Fine needle aspiration of coronal adenomas has revealed cohesive groups of nonpigmented epithelium with bland nuclei and abundant cytoplasm clustered around extracellular matrix material (Figure 5-8). [11] Ultrastructural and immunohistochemical studies indicate that the extracellular matrix material contains Type IV collagen. [12]

LEIOMYOMA
Leiomyomas of the ciliary body are rare. [13, 14, 15, 16, 17, 18] They presumably arise from ciliary muscle. The clinical diagnosis may be suggested by augmented transillumination. Electron microscopic identification of myofilaments and micropinocytotic vesicles differentiates these tumors from neurofribromas and schwannomas.
Mesectododermal leiomyomas of the ciliary body are extremely rare. [19] Fine needle aspiration characteristics of these tumors have not been reported previously. We reviewed a fine needle aspiration of one such tumor from the UCLA cytology archives. The aspirate shows tight clusters of spindle and oval cells in a fibrillary background. The nuclei are extremely bland with inconspicuous nucleoli (Figure 5-9). Sections reveal an amelanotic ciliary body mass with prominent vascularity, a fibrillary and myxoid background, and individual tumor cells that are both spindled and oval shape (Figure 5-10 and 5-11). These findings suggest a neural tumor, yet electron microscopy shows smooth muscle differentiation. [20]

MELANOCYTOMA
Melanocytoma is a benign lesion found most commonly in blacks. [21, 22] It may be found in any part of the uveal tract, but is generally present adjacent to the optic disc. Melanocytomas occasionally occur in the ciliary body. [23] The cells of a melanocytoma are large with abundant densely pigmented cytoplasm and round nuclei with small nucleoli (Figure 5-12).

ADENOMA AND CARCINOMA OF THE PIGMENTED CILIARY EPITHELIUM
Adenomas of the pigmented ciliary epithelium may clinically mimic ciliary body melanomas because they are densely pigmented (Figure 5-13). [24, 25, 26] In general, they tend to be only locally invasive. [27] Immunohistochemical studies suggest that the tumor arises from the pigmented ciliary epithelium. [28] Histologically, the tumor replaces the ciliary body and is composed of large pigmented cells arranged in a nodular pattern (Figure 5-15). Cytologic findings include large cell with abundant intracellular and extracellular pigment, and round nuclei without prominent nucleoli. [29]

References:

6. Fuchs E. Anatomische miscellen. Albrecht Von Graefes Arch Klin Ophthalmol 1883;29:209.
7. Bateman JB, Foos RY. Coronal adenomas. Arch Ophthalmol 1979;97:2379-2384.
8. Iliff W, Green WL. The incidence and histology of Fuchs’ adenoma. Arch Ophthalmol 1972;88:249-254.
9. Burch PG, Maumenee AE. Iridocyclectomy for benign tumors of the ciliary body. Am J Ophthalmol 1967;63:447-452.
10. Zaidman GW, Johnson BL, Salamon SM, Mondino BJ. Fuch’s adenoma affecting the peripheral iris. Arch Ophthalmol 1983;101:771-773.
11. Glasgow BJ. Intraocular fine needle aspiration biopsy of coronal adenomas. Diagn Cytopathol 1991;7:239-242.
12. Brown HH, Glasgow BJ, Foos RY. Coronal adenomas: ultrastructural and immunohistochemical features. Am J Ophthalmol 1991;112:34-40.
13. Blodi FC. Leiomyoma of the ciliary body. Am J Ophthalmol 1950;33:939-942.
14. Bonamour MM, Bonnet JC, Jambon M. Leiomyome du corps ciliaire; quelques considerations a propos du diagnostic et du traitement des tumeur benignes de l’iris et du corps ciliaire. Bull Soc Ophtalmol Fr 1957;7-8:482.
15. Calmettes L, Deodati F, Bec P. Leiomyome du corps ciliare. Bull Soc Ophtalmol Fr 1961;74:158-168.
16. Allen RA. Leiomyoma of ciliary body. Case presented at the Verhoeff Society, Washington, D.C., April 24-27, 1967.
17. Meyer SL, Fine BS, Front RL, Zimmerman LE. Leiomyoma of the ciliary body. Electron microscopic verification. Am J Ophthalmol 1968;66:1061-1068.
18. Calhoun FP Jr. Leiomyoma of the ciliary body. Case presented at the Verhoeff Society, Washington, D.C., April 26-29, 1976.

19. Jakobiec FA, Font RL, Tso MOM, Zimmerman LE. Mesectodermal leiomyoma of the ciliary body. A tumor of presumed neural crest origin. Cancer 1977;3 9:2102-2113.
20. Jakobiec FA, Iwamoto T. Mesectodermal leiomyoma of the ciliary body associated with a nevus. Arch Ophthalmol 1978;96:692-695.
21. Zimmerman LE. Melanocytes, melanocytic nevi, melanocytomas. Invest Ophthalmol 1965;4:11-40.
22. Reidy JJ, Apple DJ, Steinmetz RL, et al. Melanocytoma nomenclature, pathogensis, natural history and treatment. Surv Ophthalmol 1985;29:319-327.
23. Frangieh GT, El Baba F, Traboulsi El, et al. Melanocytoma of the ciliary body: presentation of four cases and review of nineteen reports. Surv Ophthalmol 1985;29:328-334.
24. Streeten BW, McGraw JL. Tumor of the ciliary pigment epithelium. Am J Ophthalmol 1972;74:420-429.
25. Wilensky JT, Holland MG. A pigmented tumor of the ciliary body. Arch Ophthalmol 1974;92:219-220.
26. Chang M, Shields JA, Wachtel DL. Adenoma of the pigment epithelium of the ciliary body simulating a malignant melanoma. Am J Ophthalmol 1979;88:40-44.
27. Anderson SR. Medulloepithelioma of the retina. In: Zimmerman LE, ed. Tumors of the eye and adnexa. Int Ophthalmol Clin 1962;2:483-506.
28. Leib WE, Shields JA, Eagle RC, Kwa D, Shields CL Cystic adenoma of the pigmented ciliary epithelium. Ophthalmol 1990;97:1489-1493.
29. Char DH, Miller TR, Crawford JB. Cytopathologic diagnosis of benign lesions simulating choroidal melanomas. Am J Ophthalmol 1991;112:70-75.



Chapter-5-page1-Abnormalities-Iris, Ciliary Body, Anterior-Chamber Angle

CHAPTER 5

Abnormalities of the Iris, Ciliary Body, and Angle Structures

In this chapter, lesions of the iris, ciliary body, and anterior chamber angle that are important in ocular cytology are illustrated. There are only a few lesions of the ciliary body, iris, and angle that are frequently ecountered in cytologic specimens. Infectious processes of the anterior chamber, iris, and ciliary body are presented in Chapter 8. Leukemias may involve the iris and shed cells into the aqueous, but are presented with other malignant neoplasms in Chapter 9. Choroidal melanomas are illustrated here.

HEMOGLOBIN SHERULOSIS AND GHOST ERYTHROCYTES

Red blood cells that have hemolyzed and hemoglobin aggregates can be identified on cytologic examination from vitrectomy and aqueous specimens [1]. Ghost erythrocytes are red blood cells in which the bulk of the hemoglobin has been extruded, leaving behind small fragments of hemoglobin festooned along the cell membrane remnants. Ghost erythrocytes are important to identify because they may enter the anterior chamber angle, obstruct the trabecular meshwork, and produce ghost-cell glaucoma [2]. Ghost-cell glaucoma has been reported after vitreous hemorrhage associated with cataract extraction or diabetic retinopathy [3].
Ghost cells appear on cytologic preparations as small ovoid to circular rings with central clear areas corresponding to the absence of hemoglobin. The hemoglobin is clumped at the periphery of the cell-forming Heinz bodies (Figure 5-1). Hemoglobin spherules are spheres of hemoglobin varying markedly in size, some of which are smaller than normal erythrocytes and others three to five times the diameter of red blood cell (Figure 5-2). Like ghost cells, hemoglobin spherules may obstruct the trabecular meshwork and produce glaucoma. If ghost cells or hemoglobin aggregates are diagnosed by cytologic examination of an aqueous, vitrectomy may be indicated in aphakic patients to relieve glaucoma [4].

PARS PLANITIS

Pars planitis is a condition in which cells and membranous veils are observed in the vitreous overlying the pars plana. This finding is termed “snowbanking.” [5] The cause of the disease is unknown. It is usually bilateral and occurs in young individuals. The collection of vitreous cells may obscure visions. Occasionally, vitrectomy may be done if an infectious agent is sought or if the opacity is chronic and severely limits vision. Histologically, lymphocytes and macrophages are seen adjacent to hyper-plastic non-pigmented ciliary epithelium. In the chronic condition, membranes may form over the pars plana composed of collagen and scare spindle cells (Figure 5-3). Perivascular sheathing of lymphocytes may also be seen (Figure 5-4). Cytologic preparations show lymphocytes and macrophages enmeshed in fibroglial membranous fragment (Figure 5-5). There finding are not specific, and the diagnosis requires careful clinical correlation.

References:
1. Grossniklaus HE, Frank KE, Farhi DC, Jacobs G, Green WR. Hemoglobin spherulosis in the vitreous cavity. Arch Ophthalmol 1988;106:961-962.
2. Campbell DG, Simmons RJ, Grant WM. Ghost cells as a cause of glaucoma. Am J Ophthalmol 1976;81:441-450.
3. Campbell DG, Essigmann EM. Hemolytic ghost cell glaucoma. Arch Ophthalmol 1979;97:2141-2146.
4. Brucker AJ, Michels RG, Green WR. Pars plana vitrectomy in the management of blood induced glaucoma with vitreous hemorrhage. Ann Ophthalmol 1978;10:1427-1437.
5. Pederson JE, Kenyon KR, Green WR, et al. Pathology of pars planitis. Am J Ophthalmol 1978;86:762-774.


Monday, September 26, 2005

Chapter-4-page2

Chapter 4-page 2
PHACOANAPHYLACTOID AND PHACOLYTIC REACTIONS

Acute traumatic lens injury may result in a release of lens protein followed by a suppurative and granulomatous inflammatory response (Figure 4-11). Cytologically, the macrophages show ingested lens material (Figure 4-12) [12]. Macrophages may obstruct the trabecular meshwork and produce elevated intraocular pressure (phacoanaphylactic glaucoma) [13]. In hypermature cataracts, lens protein may leak through the capsule without evidence of trauma and produce a macrophage inflammatory response that may obstruct the trabecular meshwork (phacolytic glaucoma) [14]. In addition, soluble lens proteins can obstruct aqueous outflow pathways and may be a factor in both of these lens-related glaucomas [15].

REFERENCE

12. Goldberg MF. Cytological diagnosis of phacolytic glaucoma utilizing Millipore filtration of the aqueous. Br J Ophthalmol 1967;51:847.
13.
Yanoff M, Scheie HG. Cytology of human lens aspirate. Arch Ophthalmol 1968;80:166-170.
14.
Flocks M, Littwin CS, Zimmerman LE. Phacolytic glaucoma. Arch Ophthalmol 1955;54:37-45.
15.
Epstein DL, Jedziniak JA, Grant MW. Obstruction of aqueous outflow by lens particles and by heavy molecular weight soluble lens protein. Invest Ophthalmol Vis Sci 1978;17:272-277.






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chapter-4-page1

CHAPTER 4

Abnormalities of the Lens

The human lens has a limited response to a wide range of noxious stimuli. The common final end point is cataract, a lenticular opacity produced by degenerative changes in crystalline proteins, Cataracts may form in different parts of the lens depending on the stimulus. Although often distinctive clinically, they are not distinguishable cytologically because the cataractous lens is emulsified by ultrasound (phacoemulsification) or chopped by a vitrectomy cutting instrument. In this chapter, those lens abnormalities that can be diagnosed by cytologic examination are illustrated.

CONGENITAL CATARACTS

There are many clinical types of congenital cataracts, including anterior polar, posterior polar zonular, sutural, membranous, and filiform. The clinical classification is based on location and slit lamp appearance. These types of cataracts cannot be distinguished in most cytologic preparations because they are generally removed by emulsifying the lens with a cutting instrument (e.g., ocutome). Despite the distortion in anatomic organization, numerous nuclei are often apparent in lens fibers of congenital cataracts obtained by emulsification (Figure 4-1) [1]. Rubella produces numerous changes in the eyes of infants, including retinopathy, nongranulomatous uveitis, glaucoma, and congenital cataract (Figure 4-2). Rubella-induced cataracts have been reported to show characteristic retention of nuclei in lens fibers (Figures 4-3 and 4-4) [2, 3, 4, 5, 6]. This feature can be seen in other types of congenital cataract [7, 8].

ADULT CATARACTS

Most adult cataracts have opacities in multiple locations within the lens. Commonly, they are opaque in both the centrally located nucleus (nuclear sclerosis or nuclear cataract)(Figure 4-5) and the peripherally located cortex (cortical cataract). Less often, opacities are present immediately beneath the capsule (subcapsular cataract). Some subcapsular cataracts are associated with trauma. Histologically, nuclear sclerotic cataracts show degenerative melding of lenticular fibers (Figure 4-6). Severely degenerated cortical lens fibers manifest as round eosinophilic globules (globular or Morgagnian degeneration). In cytologic preparations, Morgagnian globules can be identified (Figure 4-7). Sections of anterior and posterior subcapsular cataracts show a plaque of fibrous tissue and, presumably, lens epithelial cell proliferation immediately beneath the capsule (Figure 4-8) [9]. These cataracts are not usually sampled by extracapsular cataract extraction techniques.
Longstanding cataracts may become calcified [10] (cataracta calcarea) presumably by a dystrophic process [11]. In cytologic specimens, calcification appears as basophilic crystals, variable in size and shape, that exhibit birefringence (Figure 4-9 and 4-10). These crystals have been identified as calcium oxylate by x-ray diffraction and electron diffraction.


References:


1.Boniuk M. Rubella and other intraocular viral diseases in infancy. Int Ophthalmol Clin 1972;12:1-37.
2. Yanoff M, Schaffer DB, Scheie HG. Rubella ocular syndrome-clinical significance of viral and pathologic studies. Trans Am Acad Ophthalmol 1968;72:896-902.
3. Boniuk M, Zimmerman LE. Ocular pathology in the rubella syndrome. Arch Ophthalmol 1967;77:455-473.
4. Wolter JR, Insel PA, Willey EN, Brittain HP. Eye pathology following maternal rubella: a study of four children. J Pediat Ophthalmol 1966;3:29-35.
5. Zimmerman LE. The histopathologic basis for the ocular manifestations of the congenital rubella syndrome. Pro Inst Med Chicago 1968;26:170-192
6. Zimmerman LE, Font RL. Congenital malformations of the eye: some recent advances in knowledge of the pathogenesis and histopathological characteristics. JAMA 1966;196:684-692.
7. Hara J, Fujimoto F, Ishibashi T, Seguchi T, Nashimura K,et al. Ocular manifestations of the 1976 rubella epidemic in Japan. Am K Ophthalmol 1979;87:642-645.
8. Boger WP III. Late ocular complications in congenital rubella syndrome. Ophthalmology 1980;87:1244-1252.
9. Yanoff M, Fine BS. Ocular pathology, text and atlas. Philadelphia: J.B. Lippincott, 1989.
10. Harding CV, Chylack LT Jr., Susan SR, Lo W-K, Bobrowski WF, et al. Calcium containing opacities in the human lens. Invest Ophthalmol Vis Sci 1983;24:1194-1202.
11. Zimmerman LE, Johnson FB. Calcium oxalate crystals within ocular tissue. Arch Ophthalmol 1958;60:372-382.


Wednesday, September 21, 2005

Chapter-3-page5

25. Zimmerman LE. Squamous cell carcinoma and related conditions of the bulbar conjunctiva. In: Bonuik M, ed. Ocular and adnexal tumors, St. Louis: Mosby, 1964:49-74.

26. Dykstra PC, Dykstra BA. The cytologic diagnosis of carcinoma and related lesions of the ocular conjunctiva and cornea. Trans Am Acad Ophthalmol Otolaryngol 1968;73:979.

27. Irvine AR. Epibulbar squamous cell carcinoma and related lesions. Int Ophthalmol Clin 1972;12:72-83.

28. Erie JC, Campbell J, Liesegang TJ. Conjunctival and corneal intraepithelial and invasive neoplasia. Ophthalmology 1986;93:176-183.

29. McDonnell JM, McDonnell PJ, Sun YY. Polymerase chain reaction demonstration of human papillomavirus DNA in tissues and ocular surface swabs of patients with conjunctival epithelial neoplasia. Invest Ophthalmol Vis Sci 1991;32:1285.

30. Waring GO, Roth AM, Ekins MB. Clinical and pathologic description of 17 cases of corneal intraepithelial neoplasia. Am J Opthalmol 1984;97:547-559.

31. Brown HH, Glasgow BJ, Hollan GN, Foos RY, Keratinizing corneal intraepithelial neoplasia. Cornea 1989;8:220-224.

32. Robertson MC. Corneal epithelial dysplasia. Ann Ophthalmol 1984;16:1147-1150.

33. Geggel HS, Friend J, Boruchoff A. Corneal epithelial dysplasia. Ann Ophthalmol 1985;17:27-31.

34. Cameron JA, Hidayat AA. Squamous cell carcinoma of the cornea. Am J Ophthalmol 1991;111:571-574.

35. Dark AJ, Streeten BW. Preinvasive carcinoma of the cornea and conjunctiva. Br J Ophthalmol 1980;64:506-514.

36. Campbell RJ, Bourne WM. Unilateral central corneal epithelial dysplasia. Ophthalmology 1981;88:1231-1283.

37. Jakobeic FA, To WK. Corneal epithelial dysmaturation. Invest Ophthalmol Vis Sci 1991;32:1019

38. Pine L, Hardin H, Turner L, et al. Actinomycotic lacrimal canaliculitis. Am J Ophthalmol 1960;49:1278-1288.

39. Pine L, Georg LK. Reclassification of Actinomyces propionicus. Int J Syst Bacteriol 1969;19:267-272.

40. Buchanan BB, Pine L, Characterization of a propionic acid producing actinomycete. Actinomyces propionicus sp. Nov. J Gen Mircobiol 1926;28:305-323.

41. Seal DV, McGill J, Flanagan D, et al. Lacrimal canaliculitis due to Arachnia (Actinomyces) propionica. Br J Ophthalmol 1981;65:10-13.



Chapter-3-page4

REFERENCES
1. Herbert H. Pathology and diagnosis of spring catarrh. Brit Med J 1903;2:735.

2. Duggan MA, Pomponi C, Kay D, Robboy SJ. Infantile chlamydial conjunctivitis. A comparison of Papanicolaou, Giemsa and immunoperoxidase staining methods. Acta Cytol 1986;30:341-346.

3. Friedlaender MH, Okumoto M, Kelly J. Diagnosis of allergic conjunctivitis. Arch Ophthalmol 1984;102:1190-1199.

4. Hogan MJ. Atopic keratoconjunctivitis. Am J Ophthalmol 1953;36:937-947.

5. Donshik PC. Allergic conjunctivits. Int Ophthalmol Clin 1988;28:294-302.

6. Trantas A. Le catarrhe printanier en Turquie. Arch Ophtalmol (Paris) 1905;25:717-731.

7. Richmond PP, Allansmith MR. Giant papillary conjunctivitis. Int Ophthalmol Clin 1981;21:65.

8. Korb DR, Allansmith MR, Greiner JV. Prevalence of conjunctival changes in wearers of hard
contact lenses. Am J Ophthalmol 1980;90:336-341
.

9. Hatinen A, Terasvirta M, Frakj JE. Contact allergy to components in topical ophthalmologic preparations. Acta Ophthalmol (Copenh) 1985;63:424-426.

10. Butrus SI, Abelson MP. Laboratory evaluation of ocular allergy. Int Ophthalmol Clin 1988;28:324-328.

11. Abelson MB, Madiwale N, Weston JH. Conjunctival eosinophils in allergic ocular disease. Arch Ophthalmol 1983;101:555-556.

12. Thelmo W, Csordas J, Davis P, Marshall KG. The cytology of acute bacterial and follicular conjunctivits. Acta Cytol 1972;16:172-177.

13. Halberstaedter L, Von Prowazek S. Zur aetiolgie des trachoms. Dtsch Med Wochenschr 1907;33:1285-1287.

14. Wilhemus KR, Robinson NM, Tredici LL, Jones DB. Conjunctival cytology of adult chlamydial conjunctivitis. Arch Ophthalmol 1986;104:693-685.

15. Tam MR, Stamm WE, Handfield HH, Stephens R, Kuo CC, et al. Culture independent diagnosis of Chlamydia trachomatis using monoclonal antibodies. N Engl J Med 1984;320,(18):1146-1150.

16. Ugland DN, Jones DB, Wilhemus KR, et al. Diagnosis of adult chlamydial conjunctivitis by use of fluorescein-conjugated monoclonal antibody. Invest Ophthalmol Vis Sci 1985;26(suppl):272.

17. Horn JE, Kappus EW, Falkow S, Quinn TC. Diagnosis of Chlamydia trachomatis in biopsied tissue specimens by using in situ DNA hybridization. J Infect Dis 1988;157:1279-1253.

18. Horn JE, Hammer ML, Falkow S, Quinn TC. Detection of Chlamydia trachomatis in tissue culture and cervical scrapings by in situ DNA hybridization. J Infect Dis 1986;153:1155-1159.

19. Gupta PK, Shurbaji MS, Minto JL, Ermatinger SV, Myers J, et al. Cytopathologic detection of Chlamydia trachomatis in vaginopancervical (FAST) smears. Diagn Cytopathol 1988;4:224-229.

20. Ghiradini C, Ghinosi P, Raisi O, Rivasi F, Trentini GP. Detection of Chlamydia trachomatis in Papanicolaou-stained cervical smears: control study by in situ hybridization. Diagn Cytopathol 1991;7:211-214.

21. Cruess AF, Wasan SM, Willis WE. Corneal epithelial dysplasia and carcinoma in situ. Can J Ophthalmol 1981;16:171-175.

22. Ash JE, Wilder HC. Epithelial tumors of the limbus. Am J Ophthalmol 1942;25:926-931.

23. Winter FC, Kleh TR. Precancerous epithelioma of the limbus. Arch Ophthamol 1965;73:545-551.

24. Carrol JM, Kuwabara T. A classification of limbal epitheliomas. Arch Ophthalmol 1965;73:545-551.


Chapter-3-page3

CONJUNCTIVAL EPITHELIAL DYSPLASIA

Neoplasia of conjunctival epithelium is classified similarly to cervical neoplasia.[21]-25 Severity is graded by the thickness of the conjunctiva, which shows architectural and cytologic abnormalities. The criteria for dysplasia are the loss of normal cellular polarity, nuclear enlargement, nuclear irregularity, increased nucleus-to-cytoplasm size ratio, and increased numbers and abnormal forms of mitotic figures. Mild dysplasia involves up to one third of the thickness of the epithelium, moderate dysplasia up to two thirds, and severe dysplasia greater than two thirds. Carcinoma in situ is diagnosed when the entire thickness of the epithelium is involved. The clinical findings of the conjunctival and corneal hyperplasia, dysplasia, and carcinoma in situ are similar. A white epithelium with fimbriated edges and prominent blood vessels produces a surface opacity. Cytologic preparations from conjunctival dysplasia show slightly smaller conjunctival cells with hyperchromatic nuclei, an irregular chromatin pattern, and a high nucleus-to-cytoplasm ration (Figures 3-10 and 3-11). Although some authors have recommended cytologic examination of the conjunctiva as an excellent screening tool,2627 the cytologic grading of conjunctival dysplasia is not as reliable as grading of conjunctival dysplasia is not as reliable as grading of cervical disease. The reasons for this include the fact that the conjunctiva is very accessible to biopsy and assessment of margins is important in prognostication. Complete excision may be more important in determining recurrence than cell type or degree of dysplasia.28 In addition, dysplastic lesions of the conjunctiva are frequently keratinizing (Figure 3-12). Cytology from keratinized lesions often yields only surface anucleate Squamous cells so that the underlying neoplastic process may escape detection (Figures 3-13 and 3-14). Papilloma virus, especially type 16, has been identified in conjunctival swabs of many patients with conjunctival epithelial dysplasias by polymerase chain amplification. The virus is not found in all cases and its significance is yet to be elucidated.29 Intraepithelial neoplasia originating in the cornea is extremely rare. Most corneal intraepithelial dysplastic lesions are associated with limbal lesions,30 and dysplastic lesions confined to the cornea are rare.31, 32, 33, 34 Features considered precancerous in dysplastic lesions include the intracytoplasmic desmosomes, conspicuous tonofibrils, and dyskeratotic bodies and excessive basement membrane.35, 36 Clinically, hyperplastic lesions and dysplastic lesions are often distinguishable. Accurate cytologic diagnosis of hyperplasia is also difficult.37

CANALICULITIS
Inflammation of the lacrimal canaliculus that drains tears from the eye in the nasolacrimal duct is called canaliculitis. The most common cause of chronic canaliculitis is Actinomyces.38 Actinomyces israeli and Arachnia propionica (formerly Actinomyces propionicus) have been major organisms identified.39, 40, 41 The most common clinical findings are swelling of the soft tissue around the puncta and an expressible thick white exudates. Smears of the canalicular discharge show numerous neutrophils and sulfur granules composed of masses of filamentous forms with a fine branching pattern (Figure 3-15). A tissue gram stain (Brown-Brenn) is excellent for demonstrating the actinomyces organism (Figure 3-16). This method is cost effective to diagnose actinomyces canaliculitis.


References:
21. Cruess AF, et al. Can J Opthalmol, 1981.
22. Ash JE, Wilder HC. Epithelial tumors of the limbus. Am J Opthalmol 1942.
23. Winter FC, et al. Arch Opthalmol 1960.
24. Carroll JM, et al. Arch Opthalmol 1965.
25. Zimmerman LE. Squamous cell carcinoma and related conditions of the bulbar conjunctiva. In: Boniuk M, ed. Ocular and adnexal tumors, St. Louis, Mosby, 1964: 49-74.
26. Dykstra PC, Dykstra BA. The cytologic diagnosis of carcinoma and related lesions of the ocular conjunctiva and cornea. Trans Am Acad Opthalmol Otoaryngol 1968;73:979.
27. Irvine AR. Int Opthalomol Clin 1972.
28. Erie JC, et al. Opthalmology 1991.
29. McDonnell JM, McDonnell PJ, Sun YY. Polymerase chain reaction demonstration of human papilloma virus DNA in tissues and ocular surface swabs of patients with conjunctival epithelial neoplasia. Invest Opthalmol Vis Sci 1991;32;1285.
30. Waring GO, et al. Am J Opthalmol 1984.
31. Brown HH, et al. Cornea 1989.
32. Robertson MC. Corneal epithelial dysplasia. Ann Opthalmol 1984;16:1147-1150.
33. Geggel HS, et al. Ann Opthalmol 1985.
34. Cameron JA, et al. Am J Opthalmol 1991.
35. Dark AJ, et al. Br J Opthalmol 1980.
36. Campbell RJ, et al. Opthalmology 1981.
37. Jakobeic FA, to KW. Corneal epithelial dysmaturation. Invest Opthalmol Vis Sci 1991;32:1019.
38. Pine L, et al. Actinomyotic lacrimal canaliculitis Am J Syst Bacteriol 1960;49:1278-1288.
39. Pine L, Georg LK. Reclassification of Actinomyces propionicus. Int J Syst Bacteriol 1969;19:267-272.
40. Buchanan BB, et al. J Gen Microbiol 1962.
41. Seal DV, et al. Opthalmol 1981.


Chapter-3-page2

Giant papillary conjunctivitis is associated with foreign bodies, such as contact lenses, sutures, and prostheses.[7] Giant upper tarsal conjunctival papillae are arbitrarily defined as greater than 0.3 mm in diameter.[8] Contact allergic conjunctivitis may be produced by ophthalmic medications, including neomycin, bacitracin, atropine, thimerosal, benzalkonium chloride, and chloramphenical.[9] Cytologic preparations in all of these allergic disorders may show mast cells, eosinophils, and basophils (Figure 3-4). Eosinophils are not normally present in the conjunctiva; therefore, the presence of any may be significant.[10] However, eosinophils may be absent in allergic conjunctivitis.[11]

ADENOVIRUS
Acute conjunctivitis due to adenovirus infection is characterized clinically by the presence of pale nodules (follicles) in the conjunctiva, a red eye, watery discharge, and preauricular lymphadenopathy (Figure 3-5). Cytologic smears may show numerous lymphocytes of varying sizes, occasional macrophages, and epithelial cells may exhibit nuclear enlargement, an increased nuclear-to-cytoplasmic ratio and, rarely, intranuclear inclusions. Certain strains of adenovirus, types 3 and 8, may selectively infect conjunctiva.[12]

CHLAMYDIA TRACHOMATIS
Trachoma, caused by the bacterial agent Chlamydia trachomatis is a major cause of blindness in the world, in the United States, it manifests as inclusion conjunctivitis characterized by a follicular conjunctivitis (Figure 3-7). Chlamydia is important to diagnose because the disease may require topical systemic therapy. Historically, the diagnosis has been made by cytology of conjunctival scrapings.[13] Chlamydial infection begins when the elementary body, a 300 nanometer (nm) particle enters epithelial cells. This particle is enclosed by the host membrane and enlarges to become the initial body (1000 nm). The initial body divides to form numerous elementary bodies. When the cell ruptures, the cycle is continued. On Giemsa-stained preparations, the initial body is basophilic and helmet shaped (Figure 3-8). The cellular constituents seen on Giemsa-stained preparations from known chlamydia infections include neutrophils (usually predominant), lymphocytes, immunoblasts, plasma cells, and occasional multinucleated cells.[14] Because cytoplasmic inclusions are only rarely identified in patients with clinically suspected disease, classic cytology has been largely supplanted by direct immunofluorescence with fluorescein-conjugated monoclonal antibody.[15] However, false positive results may occur with this test; therefore, a combination of techniques (e.g., smear and culture) has been recommended.[16] In-situ hybridization for chlamydia has been 100% sensitive and specific in animal models.[17] However, in human tissues, the specificity and sensitivity have been reported to be only 80% and 91%, respectively.[18] Papanicolaou staining of smears in gynecologic specimens may be as effective for diagnosis as DNA in-situ hybridization.[19-20]


References:
7. Richmond PP et. al Int Opthamol Clin 1981.
8. Korb DR et. al Am J Opthalmol 1980.
9. Hatinen A. et. al Acta Opthalmol (Copenh) 1985.
10. Butrus SI. et. al Int Opthalmol Clin 1988.
11. Abelson MB et. al Arch Opthalmol 1983.
12. Thelmo W. et. al Acta Cytol 1972.
13. Halberstaedter L, Von Prowazek, S. Zur aetiolgie des trachoms. Dtsch Med Wochenschr 1907;16:172-177.
14. Wilhelmus KR, et. al Arch Opthalmol 1986.
15. Tam MR, et. al N Eng J Med 1984.
16. Ugland DN, Jones DB, Wilhelmus KR, et. al. Diagnosis of adult chlamydial conjunctivitis and use of fluorsecein-conjugated monoclonal antibody. Invest Opthalmol Vis Sci 1985;26(suppl):272.
17. Horn JE, Kappus EW, Falkow S, Quinn TC. Diagnosis of Chlamydial trachomatis in biopsied tissue speciemens using in situ DNA hybridization. J Infect Dis 1985; 157:12790-1953.
18. Horn JE, Hammer ML, Falkow S, Quinn TC. Detection of Chlamydia trachomatis in biopsied tissue soecimens by using DNA hybridization. J Infect Dis 1986; 153:1155-1159.
19. Gupta PK, et al. Diagn Cytopathol 1988.
20. Ghiradini C, et al. Diagn Cytopathol 1991.


Chapter-3-page1

CHAPTER 3

External Disease of the Conjunctiva, Cornea, and Lacrimal Drainage System

Exfoliative ocular cytology has been used effectively to identify the cell types participating in conjunctival inflammation[1] and to identify specific infectious agents, such as chlamydia.[2] Unfortunately, exfoliative cytology of the cornea and conjunctiva is less reliable for the diagnosis of neoplastic conditions. In this chapter, the utility of cytology in external ocular diseases is addressed with illustrations of selected examples.

ACUTE CONJUNCTIVITIS

Acute bacterial conjunctivitis is one of the most common causes of a red eye. The clinical finding of a red eye with mucopurulent discharge is not specific and may be seen in other conditions, including allergic conjuncttivitis. While cultures are the best means to determine a specific etiologic agent, conjunctival cytology is a simple way to confirm an acute inflammatory response. However, conjunctival cultures have certain disadvantages. They are expensive. A positive culture may not indicate pathogenicity because bacteria normally inhabit the conjunctiva and eyelid. Because many bacterial conjunctival infections are self-limited, microbial cultures are frequently superfluous. Furthermore, topical antibiotics have a broad spectrum so that initial treatment is usually based on culture results. In acute bacterial conjunctivitis, cytologic preparations show epithelial cells and numerous segmented polymorphonuclear leukocytes (Figure 3-1). These findings are not specific for bacterial conjunctivitis, but simply indicate a marked acute inflammatory response.
Gonococcal conjunctivitis is noteworthy because it requires immediate systemic treatment. Clinical findings of gonococcal conjunctivitis usually include a red eye and characteristically an intense hyperpurulent discharge. Gram stain reveals gram-negative intracellular diplococci and sheets of neutrophils. Because the disease can be fulminant, initial treatment is predicated on the results of the gram stain.

ALLERGIC CONJUNCTIVITIS

Allergic conjunctivitis includes the clinical subsets of hay fever, atopic keratoconjunctivitis, vernal conjunctivitis, giant papillary conjunctivitis, and contact allergy. All of these disorders produce symptoms of intense itching and tearing. Enlarged conjunctival papillae are seen on clinical examination (Figure 3-2).
Hay fever is the most common form of allergic conjunctivitis.[3] It is seasonal in character, mild in intensity, and shows no corneal involvement.
Atopic keratoconjunctivitis has been associated with atopic dermatitis,[4] occurs in the late teens, shows greater enlargement of papillae in the lower palpebral conjunctiva than in the upper tarsal conjunctiva, and often exhibits eyelid swelling and maceration.[5]
Vernal conjunctivitis is characterized by a seasonal predilection, propensity for elevated large cobblestone papillae of the upper tarsal conjunctiva, and grey limbal nodules called Horner-Trantas dots,[6] that are collections of eosinophils (Figures 3-3 and 3-4).

References:
1. Herbert H. Pathology and diagnosis of spring catarrh. Brit Med J 1903;2:735.
2. Duggan MA et al. Acta Cytolog. 1986
3. Friedlaender MH et al. Arch. Opthalmol. 1984
4. Hogan MJ. Am J Opthalmol. 1953
5. Donishik PC. Allerfic conjunctivitis. 1988
6. Trantas A. Le catarrhe printanier en Turquie. Arch Opthalmol 1953 (Paris) 1905;25:717-731




Ch 2 Ocular Anatomy, Retinal Pigment Epithelium, pg 4

RETINAL PIGMENT EPITHELIUM The retinal pigment epithelium is a monolayer that lies between photoreceptor outer segments and Bruch’s membrane (Figure 2-21). This epithelium has many functions, including matrix production for photoreceptors, phagocytosis or outer segments, barrier protection, and active transport. These cells are large; are polygonal in shape; and contain abundant cytoplasm, round nuclei, and single nucleoli. The cytoplasm contains large distinctive ovoid and elliptical pigment granules (Figure 2-22). The retinal pigment epithelium has a remarkable potential to proliferate and undergo metaplastic transformation. CHOROID The choroid underlies the retinal pigment epithelium and is continuous anteriorly at the ora serrata with the ciliary body. It is extremely vascular and contains a layer of capillaries, the choriocapillaris, directly under Bruch’s membrane (Figure 2-21). Numerous melanocytes are interspersed with collagen in the choroids. The choroid is not sampled in vitrectomy. However, because many uveal tumors arise from the choroids, it is quite possible to sample choroidal melanocytes in fine needle aspiration. These melanocytes have a stellate shape and contain pigment granules. The cells contain small oval nucleoli (Figure 2-23). They are usually accompanied by the fibrovascular stroma of the choroid. These cells should not be confused with melanoma cells.

REFERENCES
1. Jakobiec FA. Ocular anatomy, embryology, and teratology. Philadelphia: Harper & Row, 1982 2. Hogan MJ, Alvarado JA, Weddell JE. Histology of the human eye. Philadelphia: W.B. Saunders, 1971.
3. Last RJ. Eugene Wolff’s anatomy of the eye and orbit. Philadelphia: W.B. Saunders, 1961.
4. Fine BS, Yanoff M. Ocular histology, a text and atlas. New York: Harper and Row, 1972
5. Strenstrom S. Untersuchungen uber die variation unk kovariation der optishen elemente des menshlickhen auges. Acta Ophthalmol 1946;26:1.
6. Duke-Elder WS. The anatomy of the visual system. In: System of ophthalmology. St. Louis: CV Mosby, 1961;2:410-413
7. Greiner JV, Covington HI, Allansmith MR. Surface morphology of the human upper tarsal conjunctiva. Am J Ophthalmol 1977;83:892-905.
8. Dark AJ, Durrant TE, McGinty F, Shortland JR, et al. Tarsal conjuctiva of the upper eyelid. Am J Ophthalmol 1974;77:555-564.
9. Hogan MJ, Alvarado JA, Weddell JE. Histology of the human eye. Philadelphia: W.B. Saunders, 1971.
10. Blumcke S, Morgenroth K Jr. The stereo ultrastructure of the external and internal surface of the cornea. J Ultrastruct Res 1967;18:502.
11. Hogan et al., Histology of the human eye, 202-255.
12. Glasgow BJ. Intraocular fine needle aspiration of coronal adenomas. Diagn Cytopathol 1991;7:239-242.
13. Tolentino FI, Schepens CL, Freeman HM. Vitreoretinal disorders, diagnosis and management. Philadelphia: W.B. Saunders, 1976;1-43.
14. Sebag J, Balazs EA. Morphology and ultrastructure of human vitreous fibers. Invest Ophthalmol Vis Sci 1989;30:1867-1871.
15. Foos RY. Vitreoretinal juncture: topographical variations. Invest Ophthalmol Vis Sci 1972;10:801-808.
16. Foos RY. Anatomic and pathologic aspects of the vitreous body. Trans Am Acad Ophthalmol Otolaryngol 1973;77:OP171-OP183.
17. Gartner J. Histologische Beobachtugen uber physiologische vitreovaskulare. Adharenzen Klin Mbl Augen 1962;141:530-545.
18. Foos RY. Vitreous base, retinal tufts, and retinal tears: pathogenic relationships. In: Pruett RC and Regan CCJ, ed. Retina Congress. New York: Appleton-Century-Crofts, 1974.



Chapter 2 Anatomy- Iris, Pigment Epithelium, Retina, Vitreous

IRIS: The iris is the pigmented diaphragm separating the anterior and posterior chambers. It is joined to the ciliary body at the iris root. The anterior surface is composed of a condensed layer of fibroblasts, melanocytes, and collagen fibrils. The iris stroma contains melanocyts, fibroblasts, and blood vessels arranged in a loose network. The posterior surface of the iris is composed of two pigmented epithelial layers (Figure 2-9). The two layers have interwoven microvilli and are attached to each other laterally by desmosomes. The more anterior iris epithelial cells are fusiform in shape and extend myofilamentous cytoplasmic processes into the iris stroma (the dilator muscle). The posterior epithelial cells are columnar in shape. Both layers are densely pigmented (11). The iris is rarely sampled by cytologic techniques. However, normal iris may appear in intraocular washings from incidental ocutome cutting of the iris in an attempt to remove vitreous or lens fragments in the anterior chamber (Figure 2-10). Normal iris also may appear in fine needle aspiration specimens of iris neoplasms. In general, normal iris epithelium is so densely pigmented that cellular details are obscured (Figure 2-11). Iris stroma is characterized by the fine reticular meshwork of very cohesive and vascularized stroma. LENS: The lens is an encapsulated, biconvex structure that is suspended by thin zonules that are attached to the ciliary body . The lens epithelium is located on the internal surface of the capsule. The interior of the lens is composed of cortical and nuclear cells. These hexagonally shaped anucleate cells are joined by interdigitations (Figure 2-12). Because lens cells migrate anteriorly during embryogenesis, the posterior surface of the normal adult lens has no epithelium. Thus, the posterior surface of the lens covered only by a capsule (Figure 2-13). The lens is generally sampled during vitrectomy or lensectomy. The lens capsule can be identified on cytology preparations as a translucent (glass) membrane (Figure 2-14). This appears light green with Papanicolaou stain. Cortical fragments taken from the lens periphery or the bow sometimes demonstrate nucleated cells. Lens fragments appear as eosinophilic hexagonal structures by hemtoxylin and eosin, and light green with Papanicolaou stain (Figure 2-14). CILIARY BODY The ciliary body is composed of the ciliary processes, ciliary muscle, and ciliary epithelium (Figure 2-15). About 70 radially arranged ciliary processes form the pars plicata anteriorly and are joined posteriorly with the smooth portion of the ciliary body, the pars plana (Figure 2-1). The pars plana joins the retina and choroid at the ora serrata. The ciliary body is covered by two nonpigmented layer and an outer pigmented layer (Figure 2-16). Under normal circumstances, ciliary body structures will not appear in vitrectomy specimens. However, ciliary epithelium may be sampled by fine needle aspiration of adjacent tumors. It is important to recognize the two-layered structure of the epithelium with abundant cytoplasm and large pigmented granules (Figure 2-17) (12). VITREOUS The vitreous cavity is simply an expanded extracellular space that normally contains 4.0 ml of clear gelatinous substance that is composed largely of water, hyaluronic acid, and collagen (13). The vitreous normally contains anteroposterior oriented collagen fibrils and occasional macrophages or hyalocytes (14). The presence of even small numbers of acute or chronic inflammatory cells within the vitreous is distinctly abnormal. The vitreous has distinct attachments to ocular structures (15). It is attached anteriorly in a circumferential band extending from the posterior pars plana to a few millimeters behind the ora serrata in what has been termed the vitreous base. Traction exerted by the vitreous body at the base results in hyperpigmentation of the underlying pigment epithelium and is evident grossly (16) (Figure below).




click on photo for a larger image

Above -dark pigmentation on the anterior border of the vitreous base (VB).


Below- transillumination highlights the pigmentation of the vitreous base as it straddles the ora serrata.


The vitreous is also attached to the retina over retinal blood vessels and at the optic disc (17). These attachments are important to understanding vitreous traction, retinal tears, and retinal detachment, for which vitrectomies are sometimes performed.

RETINA The sensory neuroepithelium of the eye is the retina, which is composed of many layers (Figure 2-18). These include the layer of outer and inner segments of the photoreceptor cells, the outer nuclear layer (cell bodies of photoreceptor cells), the outer plexiform layer, the inner nuclear layer, the inner plexiform layer, the ganglion cell layer, the nerve fiber layer, and the inner limiting lamina (membrane). The retina is loosely attached to the pigment epithelium, which is separated from the choroids by Bruch’s membrane. Normal and abnormal retina and pigment epithelium may be sampled in both vitrectomy and fine needle aspiration. In vitrectomy, the retina may be removed inadvertently. In cytologic preparations, the retina usually appears as a plexiform pattern of cells with round nuclei and characteristic organoid architecture (Figure 2-19). Often only small fragments of retinal tissue will be present, but can be recognized by the organoid architecture and distinctive nuclear halos (Figure 2-20). Occasionally, ganglion cells may be sampled (Figure 2-19). It is important for the cytologist to report retinal fragments discovered in intraocular washings because full thickness breaks in the retina may lead to retinal detachment. If the surgeon is made aware, the breaks may be closed with cryotherapy, laser, gas injection, or scleral buckle. Fragments of partial-thickness retina that have been stripped in the process of peeling membranes from the retinal surface are not uncommon in intraocular washings and are not regarded presently as clinically significant.

References:

11. Hogan et al., Histology of the human eye, 202-255.

12. Glasgow BJ. Intraocular fine needle aspiration of coronal adenomas. Diagn Cytopathol 1991;7:239-242.
13. Tolentino FI, Schepens CL, Freeman HM. Vitreoretinal disorders, diagnosis and management. Philadelphia: W.B. Saunders, 1976;1-43.

14. Sebag J, Balazs EA. Morphology and ultrastructure of human vitreous fibers. Invest Ophthalmol Vis Sci 1989;30:1867-1871.

15. Foos RY. Vitreoretinal juncture: topographical variations. Invest Ophthalmol Vis Sci 1972;10:801-808.

16. Foos RY. Anatomic and pathologic aspects of the vitreous body. Trans Am Acad Ophthalmol Otolaryngol 1973;77:OP171-OP183.

17. Gartner J. Histologische Beobachtugen uber physiologische vitreovaskulare. Adharenzen Klin Mbl Augen 1962;141:530-545.

Introduction to Ocular Cytopathology



The aim of this book is to provide pathologists, ophthalmologists, and students of ophthalmic pathology with an understanding of the appearance of fundamental lesions of ocular cytology. There is emphasis on techniques used to obtain and process laboratory specimens. Clinical and radiologic appearances are stressed where relevant to cytologic interpretation.
A general section of ocular anatomy may be quite helpful. This book includes sections on exfoliative cytology of the eye, intraocular washings and fine needle aspiration of the eye and the orbit. It is not intended to be a detailed exposition of all ocular diseases. Rather this atlas serves as a practical guide with information needed to interpret common eye cytology specimens. It is written for the general pathologist/cytologist with little in depth training in eye disease who is asked to interpret ocular specimens. Abundant clinical, radiologic and histologic material is presented to provide a general perspective for those with little previous experience in ophthalmology.
Hopefully this book will provide a valuable resource for clinicians faced with diagnostic problems that may be solved by cytologic techniques. In addition, detailed information regarding processing will assist clinicians to choose appropriate investigative techniques. Students of ophthalmic pathology will find this atlas useful to learn the basics of eye cytology and to apply knowledge of histology to cytologic features of eye diseases. To aid in this transition, numerous color gross and microscopic photographs are presented in the printed version.

In the version currently presented on line we have provide links to illustrations and simulated microscopy. In time we will replace these with links to high quality photomicrographs from the atlas.

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Tuesday, September 20, 2005

Ocular Cytopathology Table of Contents & Ch 1