Ординатура / Офтальмология / Английские материалы / Textbook of Vitreoretinal Diseases and Surgery_Natarajan, Hussain_2008
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Textbook of Vitreoretinal Diseases and Surgery
Unlike the above-mentioned methods, when a perfluorocarbon liquid is used, the drainage sclerotomies should be placed anteriorly, approximately 4 mm off the limbus. A 30-gauge needle attached to a syringe containing perfluorocarbon liquid is then introduced through the limbus. This liquid material is then slowly injected, whereby it will immediately move posteriorly. As it fills the posterior chamber, the per fluorocarbon liquid will flatten the posterior pole while displacing suprachoroidal blood anteriorly, thereby allowing more complete removal of liquefied blood through anteriorly placed sclerotomies (Figures 11-3 and 11-4).
Prognosis
EXPULSIVE SUPRACHOROIDAL HEMORRHAGE
In cases of expulsive SCH, in the absence of a rhegmatogenous retinal detachment, both early surgical intervention and observation and medical management have been advocated. It does not appear that all patients suffering from an expulsive SCH should be subjected to a secondary surgical procedure. Secondary surgery, however, should be contemplated on an individual level, based on clearly defined indications or intervention.
DELAYED SUPRACHOROIDAL HEMORRHAGE
Abrams et al reported the greatest success with early surgical drainage in patients with delayed SCH.41 In theirstudy,three ofsevenpatients maintainedprehemorrhagevisual acuity, and twoofsevenpatients actually had a final visual acuity that was better than their prehemorrhage visual acuity.
FIGURE 11-3: Showing egression of dark colored suprachoroidal blood through the sclerotomies under infusion through the anterior chamber maintainer. Surgery was performed after liquefaction of suprachoroidal
128 blood seen on B-scan as shown in Figures 11-1 and 11-2 (Courtesy: Dr Nazimul Hussain, Al Zahra Pvt Hospital, UAE)
Suprachoroidal Hemorrhage
FIGURE 11-4: Fundus photograph of the same patient (Figures 11-1 to 11-3) after vitreoretinal surgery for expulsive hemorrhage. Note the attached retina under silicone oil (Courtesy: Dr Nazimul Hussain, Al Zahra Pvt Hospital, UAE)
New Frontiers
A new treatment modality is the use of intravenous tissue plasminogen activator to accelerate clot lysis.42 This form of treatment is experimental, and its clinical benefit remains to be proved. Finally, the use of silicone oil tamponade after vitreoretinal surgery for SCH has been recommended, but should be reserved for only the most desperate cases.
References
1.Pfingst AO. Expulsive choroidal hemorrhage complicating cataract surgery. South Med J 1936;29:323.
2.Terson A. Hemorragies sous-choroidiennes traumatiques et expulsives. Arch Ophtalmol 1907;27:446.
3.Verhoeff FH. Scleral puncture for expulsive subchoroidal hemorrhage following sclerotomy: scleral puncture for postoperative separation of the choroid. Ophthalmic Res 1915;24:55–9.
4.Brubaker RF, Pederson JE. Ciliochoroidal detachment. Surv Ophthalmol 1983;27:281–9.
5.Hawkins WR, Schepens CL. Choroidal detachment and retinal surgery. Am J Ophthalmol 1966;62:813–9.
6.Davison JA. Acute intraoperative suprachoroidal hemorrhage in extracapsular cataract surgery. J Cataract Refract Surg 1986;12:606–22.
7.AugsburgerJJ,CoatsTD,LauritzenK.Localizedsuprachoroidalhematomas:Ophthalmoscopicfeatures,fluorescein angiography, and clinical course. Arch Ophthalmol 1990;108: 968–72.
8.Hoffman P, Pollack A, Oliver M. Limited choroidal hemorrhage associated with intracapsular cataract extraction. Arch Ophthalmol 1984;102:1761–5.
9.Manschot WA. The pathology of expulsive hemorrhage. Am J Ophthalmol 1955;40:15–24.
10.Maumenee AE, Schwartz MF. Acute intraoperative choroidal effusion. Am J Ophthalmol 1985;100:147–54.
11.Zauberman H. Expulsive choroidal haemorrhage: an experimental study. Br J Ophthalmol 1982;66:43–5.
12.BeyerCF,PeymanGA,HillJM.Expulsivechoroidalhemorrhageinrabbits:Ahistopathologicstudy.ArchOphthalmol 129 1989;107:1648–53.
Textbook of Vitreoretinal Diseases and Surgery
13.Wolter JR,Garfinkel RA. Ciliochoroidal effusion as precursor of suprachoroidal hemorrhage: a pathologic study. Ophthalmic Surg 1988;19:344–9.
14.Payne JW, Kameen AJ, Jensen AD, Christy NE. Expulsive hemorrhage: its incidence in cataract surgery and a report of four bilateral cases. Trans Am Ophthalmol Soc 1985;83:181–204.
15.SpeakerMG,GuerrieroPN,MetJA,etal.Acase-controlstudyofriskfactorsforintraoperativesuprachoroidalexpulsive hemorrhage. Ophthalmology 1991;98:202–10.
16.Taylor DM. Expulsive hemorrhage. Am J Ophthalmol 1974;78:961–6.
17.Duehr PA, Hogenson CD. Treatment of subchoroidal hemorrhage by posterior sclerotomy. Arch Ophthalmol 1947;38:365–7.
18.DavisonJA.Acuteintraoperativesuprachoroidalhemorrhageincapsularbagphacoemulsification.JCataractRefract Surg 1993;19:534–7.
19.Gressel MG, Parrish RK II, Heuer DK. Delayed nonexpulsive suprachoroidal hemorrhage. Arch Ophthalmol 1984;102:1757–60.
20.GivensK,ShieldsMB.Suprachoroidalhemorrhageafterglaucomafilteringsurgery.AmJOphthalmol1987;103:68-94.
21.TabandehH,SullivanPM,SmahliukP,etal.Suprachoroidalhemorrhageduringparsplanavitrectomy.Ophthalmology 1999;106:236–42.
22.RudermanJM,HarbinTSJr,CampbellDG.Postoperativesuprachoroidalhemorrhagefollowingfiltrationprocedures. Arch Ophthalmol 1986;104:201–5.
23.ChorichLJ,DerickRJ,ChambersRB.Hemorrhagicocularcomplicationsassociatedwiththeuseofsystemicthrombolytic agents. Ophthalmology 1998;105:428–31.
24.Khawly JA, Ferrone PJ, Holck DE. Choroidal hemorrhage associated with systemic tissue plasminogen activator. Am J Ophthalmol 1996;121:577–8.
25.Blumenthal M, Grinbaum A, Assia EI. Preventing expulsive hemorrhage using an anterior chamber maintainer to eliminate hypotony. J Cataract Refract Surg 1997;23:476–9.
26.LakhanpalV,SchocketSS,ElmanMJ,NirankariVS.Anewmodifiedvitreoretinalsurgicalapproachinthemanagement of massive suprachoroidal hemorrhage. Ophthalmology 1989;96:793–800.
27.GloorB,KalmanA.Chorioidaleffusionundexpulsiveblutangbeibulbuseroffnendeneingriffen:lehrenvon26patienten. Klin Monatsbl Augenheilkd 1993;202:224–37.
28.OssoinigKC.Standardizedechography:basicprinciples,clinicalapplications,andresults.IntOphthalmolClin1979;19: 127–210.
29.Nasr A, Ossoinig KC, Weingeist TA. The importance of standardized echography in the assessment of post surgical suprechoroidal detachment, in Ossoinig KC (Ed): Ophthalmic Echography Dordrecht, the Netherlands, Martinus Nijhoff, 1987;345–46.
30.Chu TG, Cano MR, Green RL. Massive suprachoroidal hemmorrhage with central retinal apposition: A clinical and echographic study. Arch Ophthalmol 1991;109:1575–81.
31.GloorB,KalmanA.Chorioidaleffusionundexpulsivebluntingbeibulbuseroffnendeneingriffen:lehrenvon26patienten Klin Monatsbl Augenheilkd 1993;202:224–37.
32.Welch JC, Spaeth GL, Benson WE. Massive suprachoroidal hemorrhage: Follow-up and outcome of 30 cases. Ophthalmology 1988;95:1202–6.
33.Lambrou FH Jr, Meredith TA, Kaplan HJ. Secondary surgical management of expulsive choroidal hemorrhage. Arch Ophthalmol 1987;105:1195–8.
34.PeymanGA,MafeeM,SchulmanJ.Computedtomographyinchoroidaldetachment.Ophthalmology1984;91:156-62.
35.Mafee MF, Linder B, Peyman GA, et al. Choroidal hematoma and effusion: evaluation with MR imaging. Radiology 1988;168:781–6.
36.BecquetF,CaputoG,MashhourB.Managementofdelayedmassivesuprachoroidalhemorrhage:aclinicalretrospective study. Eur J Ophthalmol 1996;6:393–7.
37.Verhoeff FH. Scleral puncture for expulsive subchoroidal hemorrhage following sclerotomy: scleral puncture for post operative separation of the choroid. Ophthalmic Res 1915;24:55–9.
38.Baldwin LB, Smith TJ, Hollins JL, Pearson PA. The use of viscoelastic substances in the drainage of postoperative suprachoroidal hemorrhage [see comments]. Ophthalmic Surg 1989;20:504–7.
39.Davison JA. Vitrectomy and fluid infusion in the treatment of delayed suprachoroidal hemorrhage after combined cataract and glaucoma filtration surgery. Ophthalmic Surg 1987;18: 334–6.
40.Desai UR, Peyman GA, Chen CJ. Use of perfluoroperhydrophenanthrene in the management of suprachoroidal hemmorrhages. Ophthalmology 1992;99:1542–7.
41.Abrams GW, Thomas MA, Williams GA, Burton TC. Management of post operative suprachoroidal hemmorrhage with continuous infusion air pump. Arch Ophthalmol 1986;104:1455-8.
42.Liu JC, Peyman GA, Oncel M. Treatment of experimental suprachoroidal hemorrhage with intravenous tissue
130 plasminogen activator. Int Ophthalmol 1990;14:267–70.
Textbook of Vitreoretinal Diseases and Surgery
Introduction
Posterior uveitis is a group of disorders, which often pose diagnostic and therapeutic dilemma to the treating ophthalmologist. In the management of posterior uveitis it is required to ascertain the cause of the posterior segment inflammation, its stage and extent and also its contribution to the associated visual loss. A number of techniques are used to image the posterior segment in a patient with uveitis.
Imaging techniques in uveitis are used:
1.To determine the presence or absence of specific uveitic diseases with characteristic patterns as seen on imaging.
2.To determine the stage of activity of the specific disease and the extent of involvement of the posterior segment.
3.To determine the cause of the vision loss in the affected eye.
In this chapter, we shall try to understand the basis and the indications for use of imaging
techniques in the management of posterior uveitis.
The Technique
The techniques used for imaging the posterior segment in uveitis are as follows:
COLOR FUNDUS PHOTOGRAPHY
The first tool that can be used to document the presence of a fundus lesion at the initial visit and to further judge the extent and progression of the disease in the subsequent follow up visits is digital color fundus photography (Figures 12-1A to D). Digital fundus photography has the added advantage of simple storage and retrieval of images over the conventional film-based colour fundus photography. The construction of a composite montage further enhances the documentation of the extent of the lesion in the peripheral fundus. A good agreement has been found among the uveitis specialists on the interpretation of retinal photographs of patients with presumed Toxoplasma chorioretinitis.1
FUNDUS FLUORESCEIN ANGIOGRAPHY (FFA)
In patients with posterior uveitis, FFA is useful to detect and document vasculitis and subsequent areas of peripheral capillary non-perfusion (Figure 12-2) in Eales’ disease, Intermediate uveitis, Sarcoidosis, and also in uncommon conditions like Behcet’s disease.2 Further it can be used to show leakage of dye from inflamed retinal capillaries at the macula (Cystoid Macular edema—Flower Petal pattern) (Figure 12-3) and in the optic disc (Optic Disc Edema). Lastly, it can also be used to recognize choroidal neovascularization in patients of uveitis.
INDOCYANINE GREEN ANGIOGRAPHY (ICG)
ICG provides visual access to the choroidal circulation and thus provides an insight into the understanding of the pathogenesis of various inflammatory disorders especially the white dot syndromes. The normal background choroidal fluorescence is altered in posterior uveitis as seen in the late phases of the angiogram.3 Two definite patterns of inflammatory involvement of the choroidal vessels have been reported using ICG.4,5 These are Type 1 (Figures 12-4A to D) which appears as
132 hypofluorescence in both the mid and late phases of the angiogram and is seen in the white dot
Imaging in Posterior Uveitis
FIGURES 12-1A to D: Serial color fundus photographs to document the resolution of lesions in a patients with Toxoplasma chorioretinitis. (A) 1st day, (B) 3rd day, (C) 2nd week, (D) 6th week
FIGURE 12-2: Fundus fluoresceing angiography of a patient with Eales' disease to |
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document perivasculitis, capillary non-perfusion and NVE |
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Textbook of Vitreoretinal Diseases and Surgery
FIGURE 12-3: Fundus fluorescein angiography of a patient with cystoid macular edema showing typical 'flower petal pattern' due to leakage of dye from the inflamed retinal capillaries at the macula
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FIGURES 12-4A to D: Indocyaneen green angiograph of a patient with |
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MEWDS and type 1 choroidal neovascular membrane |
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Imaging in Posterior Uveitis
syndrome where there is a selective involvement of the choriocapillaris. Disorders like tuberculosis, sarcoidosis and Vogt-Koyanagi-Harada (VKH) disease, sympathetic ophthalmia, Birdshot chorioretinopathy, Behçet’s disease and posterior scleritis affect the choroids more diffusely demonstrate the type 2 pattern characterized by late leakage of the ICG dye from the inflamed choroidal vessels.
B-SCAN ULTRASONOGRAPHY AND ULTRASOUND BIOMICROSCOPY (UBM)
B-scan ultrasonography is useful to image the posterior segment when clinical examination is not possible because of hazy media due to various causes. In uveitis, this may be due to corneal scars, hypopyon, cataract, small pupils, and pupillary membranes. In the presence of ocular hypotony in uveitis it can be used to detect choroidal detachment in the presence of opaque media. UBM uses a higher frequency probe to image the ciliary body and the pars plana region to look for ciliary body effusion or to find the cause of hypotony such as ciliary body thinning, cyclitic membranes or to document exudates in the pars plana region in cases of pars planitis with hazy media or small pupils precluding the view of the pars plana region.6 Some authors have used UBM to document the peripheral fundus involvement in toxocariasis7 and to differentiate pars planitis characterized by typical UBM pars plana deposits from Behçet’s disease, which does not show the deposits in the presence of opaque media.8 In patients who have a clear media like VKH and posterior scleritis, B scan is used to demonstrate choroidal thickening which is peripapillary to begin with (Figure 12-5) and also echolucency in the posterior sub-Tenons space (Figure 12-6).
OPTICAL COHERENCE TOMOGRAPHY (OCT)
OCT is best suited for measurement of the foveal thickness in the diagnosis and follow-up of patients with cystoid macular edema.9 OCT can also be used to document epiretinal membranes and subtle vitreomacular traction and other clinical features which are subtle on clinical examination (Figures 12-7 and 12-8).
Having an overview of the various imaging modalities used in management of posterior uveitis, we can now discuss how each of these modalities is useful to document findings in patients of uveitis with an inflammatory response causing loss of vision. We know that vision loss in a patient with uveitis is due to a myriad of causes including cystoid macular edema (CME) (Figure 12-9), optic disc inflammation, exudative neurosensory detachment, retinal phlebitis, macular retinal vascular
FIGURE 12-5: B-scan of a patient with Vogt-Koyanagi-Harada disease |
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showing choroidal thickening and multi-focal retinal detachments |
Textbook of Vitreoretinal Diseases and Surgery
FIGURE 12-6: B-scan of a patient with posterior scleritis showing echolucent area just posterior to sclera—T sign
FIGURE 12-7: Optical coherence tomography of a patient with necrotizing retinitis to document macular hole
occlusion, peripheral retinal vascular occlusion, neovascularization of the disc and elsewhere, rubeosis of the iris and angle, choroidal neovascularization and posterior scleritis.
Cystoid Macular Edema (CME)
136 FFA and OCT are the preferred imaging modalities to demonstrate the presence of CME in a patient with uveitis. Break down of the blood retinal barrier causing CME is seen in the late phases of the
Imaging in Posterior Uveitis
FIGURE 12-8: Optical coherence tomography of the same patient to document resolution of macular hole
FIGURE 12-9: Optical coherence tomography to document cystoid macular |
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edema in a patient with pars planitis |