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VOGT-KOYANAGI-HARADA DISEASE

Содержание

Multisystem diseaseChronic, bilateral, granulomatous panuveitis associated with central nervous system, auditory and integumentary manifestations VKH DiseaseMoorthy et al: Surv Ophthalmol 1995; 39:265 (review)Read et al: Am J Ophthalmol 2001;131:647

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Слайд 1VOGT-KOYANAGI-HARADA DISEASE
AHMED M. ABU EL-ASRAR, MD, PhD


Department of Ophthalmology, College

of Medicine, King Saud University, Riyadh, Saudi Arabia

Dr. Nasser Al-Rashid Research Chair in Ophthalmology
VOGT-KOYANAGI-HARADA DISEASEAHMED M. ABU EL-ASRAR, MD, PhD Department of Ophthalmology, College of Medicine, King

Слайд 2Multisystem disease
Chronic, bilateral, granulomatous panuveitis associated with central nervous system,

auditory and integumentary manifestations


VKH Disease
Moorthy et al: Surv

Ophthalmol 1995; 39:265 (review)
Read et al: Am J Ophthalmol 2001;131:647

Multisystem diseaseChronic, bilateral, granulomatous panuveitis associated with central nervous system, auditory and integumentary manifestations VKH DiseaseMoorthy

Слайд 3VKH Disease
Individuals with a predisposing genetic background.
Ethnic groups with more

heavily pigmented skin.
Asians, Native Americans, Hispanics, Asian Indians, Middle Easterners.
Epidemiology

VKH DiseaseIndividuals with a predisposing genetic background.Ethnic groups with more heavily pigmented skin.Asians, Native Americans, Hispanics, Asian

Слайд 4VKH Disease
Genetic background rather than degree of skin pigmentation.
Women more

than men.
3rd – 4th decade.
Pediatric age group.
Epidemiology
Read et al: Curr

Opin Ophthalmol 2000;11:437 (review)
Abu El-Asrar et al: Eye 2008;22:1124
Martin et al: Retina 2010 Feb 17. [Epub ahead of print]
VKH DiseaseGenetic background rather than degree of skin pigmentation.Women more than men.3rd – 4th decade.Pediatric age group.EpidemiologyRead

Слайд 5VKH Disease
Remains unknown.
T-lymphocyte mediated autoimmunity directed against one or more

antigens found on or associated with melanocytes found in eye,

skin and hair, inner ear, CNS.

Etiology and Pathogenesis

Okada et al: Graefe’s Arch Clin Exp Ophthalmol 1996;234:359

VKH DiseaseRemains unknown.T-lymphocyte mediated autoimmunity directed against one or more antigens found on or associated with melanocytes

Слайд 6VKH Disease
Tyrosinase family proteins are enzymes for melanin formation and

are expressed in melanocytes.
T-lymphocytes from VKH disease patients proliferate in

response to tyrosinase, TRP1 or TRP2.
Immunization of Lewis rats with tyrosinase, TRP1 or TRP2 produced an inflammatory disease that resembled VKH disease with skin lesions and meningitis.

Yamaki et al: J Immunol 2000;165:7323
Yamaki et al: Exp Eye Res 2000;71:361

Etiology and Pathogenesis

VKH DiseaseTyrosinase family proteins are enzymes for melanin formation and are expressed in melanocytes.T-lymphocytes from VKH disease

Слайд 7VKH Disease
Th cells from peripheral blood of VKH patients produce

predominantly Th1 cytokines (IFN-gamma, IL-2) especially when stimulated
T-cell clones specific

to tyrosinase family proteins established from peripheral blood mononuclear cells of patients with VKH disease showed proliferative responses to tyrosinase and/or TRP1 and produced Th1-type cytokines.

Imai et al: Curr Eye Res 2001;22:312
Gocho et al: Invest Ophthalmol Vis Sci 2001;42:2004

Etiology and Pathogenesis

VKH DiseaseTh cells from peripheral blood of VKH patients produce predominantly Th1 cytokines (IFN-gamma, IL-2) especially when

Слайд 8VKH Disease
IL-23 stimulated production of IL-17 by CD4+

T cells may be responsible for the development of VKH

disease.

Fang and Yang: Curr Eye Res 2008;33:517

Etiology and Pathogenesis

VKH DiseaseIL-23 stimulated production of IL-17 by CD4+ T cells may be responsible for the

Слайд 9VKH Disease
VKH-like disease in patients treated with interferon-alpha and ribavirin

therapy for chronic hepatitis

C virus infection.

Al-Muammar et al: Int Ophthalmol 2010 Feb 23. [Epub ahead of print]
Sene et al: World J Gastroenterol 2007;13:3137
Touitou et al: Am J Ophthalmol 2005;140:949
Papastathopoulos et al: J Infect 2006;52:e59
Kasahara et al: J Gastroenterol 2004;39:1106
Sylvestre et al: J Viral Hepat 2003;10:467

Etiology and Pathogenesis

VKH DiseaseVKH-like disease in patients treated with interferon-alpha and ribavirin therapy for

Слайд 10VKH Disease
Granulomatous panuveitis.
Lymphocytes, epitheloid cells, few plasma cells, multinucleated giant

cells.
Epitheloid cells and giant cells contain melanin pigment.

Pathology

VKH DiseaseGranulomatous panuveitis.Lymphocytes, epitheloid cells, few plasma cells, multinucleated giant cells.Epitheloid cells and giant cells contain melanin

Слайд 11VKH Disease
Dalen-Fuchs’ nodules: Lymphocytes, epitheloid cells, pigment-laden macrophages, altered and/or

proliferated RPE cells.
Melanocytes disappear from choroid.

Perry and Font: Am J

Ophthalmol 1977;83:242
Inomata and Rao: Am J Ophthalmol 2001;131:607

Pathology

VKH DiseaseDalen-Fuchs’ nodules: Lymphocytes, epitheloid cells, pigment-laden macrophages, altered and/or proliferated RPE cells.Melanocytes disappear from choroid.Perry and

Слайд 12VKH Disease
Certain racial groups.
Immunogenetic predisposition.
Strong association with HLA-DR4 and HLA-DRw53

with the most significant risk allele being HLA-DRB1*0405.
Causative pathogenic

antigen binds with HLA-DRB1*0405 molecule which presents the antigen to T cells to activate them.

Fang and Wang: Curr Eye Res 2008;33:517 (review).
Read et al: Curr Opin Ophthalmol 2000;11:437 (review).
Yamaki et al: Int Ophthalmol Clin 2002;42:13 (review).

Genetic Factors

VKH DiseaseCertain racial groups.Immunogenetic predisposition.Strong association with HLA-DR4 and HLA-DRw53 with the most significant risk allele being

Слайд 13VKH Disease
VKH disease in monozygotic twins
Familial VKH disease
Familial cases shared

HLA-DR4

Itho et al: Int Ophthalmol 1992;16:49
Rutzen et al:

Am J Ophthalmol 1995;119:239
Sonoda et al: Jpn J Ophthalmol 1999;43:113

Genetic Factors

VKH DiseaseVKH disease in monozygotic twinsFamilial VKH diseaseFamilial cases shared HLA-DR4 Itho et al: Int Ophthalmol 1992;16:49

Слайд 14VKH Disease
Integumentary Manifestations
Sensitivity of hair and skin to touch (early

in prodromal phase).
Poliosis, vitiligo, alopecia (during convalescent stage).
Ethnic groups may

manifest varying systemic symptoms.

Clinical Features Extraocular Manifestations

VKH DiseaseIntegumentary ManifestationsSensitivity of hair and skin to touch (early in prodromal phase).Poliosis, vitiligo, alopecia (during convalescent

Слайд 15Clinical Features Extraocular Manifestations
VKH Disease
Neurologic Manifestations
Most common during prodromal stage.
Neck stiffness,

headache, confusion.
Occasionally focal neurologic signs.
CSF pleocytosis.


Clinical Features Extraocular ManifestationsVKH DiseaseNeurologic ManifestationsMost common during prodromal stage.Neck stiffness, headache, confusion.Occasionally focal neurologic signs.CSF pleocytosis.

Слайд 16VKH Disease
Clinical Features Extraocular Manifestations
Auditory Manifestations
May be presenting problem
Sensorineural hearing loss

usually involves higher frequencies
Tinnitus
Vertigo
May cause permanent hearing loss

VKH DiseaseClinical Features Extraocular ManifestationsAuditory ManifestationsMay be presenting problemSensorineural hearing loss usually involves higher frequenciesTinnitusVertigoMay cause permanent

Слайд 17VKH Disease
Clinical Features Auditory Manifestations

VKH DiseaseClinical Features Auditory Manifestations

Слайд 18VKH Disease
4 phases
Prodromal
Acute uveitic
Convalescent or chronic

Chronic recurrent
Clinical Course

VKH Disease 4 phases Prodromal Acute uveitic Convalescent or chronic Chronic recurrentClinical Course

Слайд 19VKH Disease
Prodromal Phase:
Mimics viral illness
Neurologic and auditory manifestations
Few days
Headache, orbital

pain, stiff neck, malaise, abdominal pain, nausea, fever, vertigo, tinnitus
Cranial

nerve palsies, optic neuritis (rare)
CSF pleocytosis

Clinical Course

VKH DiseaseProdromal Phase:Mimics viral illnessNeurologic and auditory manifestationsFew daysHeadache, orbital pain, stiff neck, malaise, abdominal pain, nausea,

Слайд 20VKH Disease
Acute Uveitic Phase:
Bilateral in 70% of patients, delay of

1-3 days before 2nd eye becomes involved in 30%. In

a few cases this interval may last up to 10 days.
Hallmark is bilateral multifocal exudative retinal detachments, hyperemia and edema of the optic disc.

Clinical Course

VKH DiseaseAcute Uveitic Phase:Bilateral in 70% of patients, delay of 1-3 days before 2nd eye becomes involved

Слайд 21VKH Disease
Acute Uveitic Phase: (cont.).
Yellow-white lesions at level of RPE

beneath serous RD.
Thickening of posterior choroid manifested by elevation of

peripapillary retino-choroid layer.
Retinal edema in posterior pole.
Peripheral well-circumscribed yellow-white lesions (clinical equivalent of Dalen-Fuchs’ nodules).

Clinical Course

VKH DiseaseAcute Uveitic Phase: (cont.).Yellow-white lesions at level of RPE beneath serous RD.Thickening of posterior choroid manifested

Слайд 22VKH Disease
Acute Uveitic Phase: (cont.)
No inflammation of the anterior segment

or mild to moderate nongranulomatous anterior uveitis if the disease

is not well controlled with appropriate treatment during the first two weeks.

Clinical Course

Fang and Yang: Curr Eye Res 2008;33:517 (review)

VKH DiseaseAcute Uveitic Phase: (cont.)No inflammation of the anterior segment or mild to moderate nongranulomatous anterior uveitis

Слайд 23VKH Disease
Acute Uveitic Phase: (cont.).
Shallow anterior chamber
Elevated IOP
Acute angle closure

glaucoma

Clinical Course

VKH DiseaseAcute Uveitic Phase: (cont.).Shallow anterior chamberElevated IOPAcute angle closure glaucomaClinical Course

Слайд 24VKH Disease
Convalescent Phase:
Integumentary and uvea depigmentation.
Perilimbal vitiligo (Sugiura’s sign).
Fundus exhibits

an orange-red discoloration (“sunset-glow” fundus).

Clinical Course

VKH DiseaseConvalescent Phase:Integumentary and uvea depigmentation.Perilimbal vitiligo (Sugiura’s sign).Fundus exhibits an orange-red discoloration (“sunset-glow” fundus).Clinical Course

Слайд 25VKH Disease
Convalescent Phase: (cont.)
Multiple small yellow well-circumscribed areas of chorioretinal

atrophy representing regressed Dalen-Fuchs’ nodules.
RPE clumping or migration.
Pigmented demarcation lines.
Clinical

Course
VKH DiseaseConvalescent Phase: (cont.)Multiple small yellow well-circumscribed areas of chorioretinal atrophy representing regressed Dalen-Fuchs’ nodules.RPE clumping or

Слайд 26VKH Disease
Chronic Recurrent Phase:
Acute episodes of granulomatous anterior uveitis with

development of iris nodules
Recurrent posterior uveitis is distinctly uncommon
Complications are

seen in this phase

Clinical Course

VKH DiseaseChronic Recurrent Phase:Acute episodes of granulomatous anterior uveitis with development of iris nodulesRecurrent posterior uveitis is

Слайд 27VKH Disease
Chronic Recurrent Phase:
Patients with recurrent VKH disease had a

more intensive inflammation in the anterior segment and long-lasting dysfunction

of the blood-aqueous barrier than those with initial onset VKH disease.

Clinical Course

Fang et al: Br J Ophthalmol 2008;92:182

VKH DiseaseChronic Recurrent Phase:Patients with recurrent VKH disease had a more intensive inflammation in the anterior segment

Слайд 28VKH Disease
Fluorescein angiography
Indocyanine green angiography
Ultrasonography
Optical coherence tomography
Multifocal electroretinograms
Lumbar puncture

Laboratory Investigations
Diagnosis

is made by clinical examination and ancillary test findings

VKH DiseaseFluorescein angiographyIndocyanine green angiographyUltrasonographyOptical coherence tomographyMultifocal electroretinogramsLumbar punctureLaboratory Investigations Diagnosis is made by clinical examination and

Слайд 29VKH Disease
Ultrasonography:
Diffuse low to medium thickening of choroid.
Overlying exudative RD.
Laboratory

Investigations

VKH DiseaseUltrasonography:Diffuse low to medium thickening of choroid.Overlying exudative RD.Laboratory Investigations

Слайд 30VKH Disease
Laboratory Investigations
OCT
Useful in monitoring resolution of exudative retinal detachment
On

presentation
4 weeks after systemic corticosteroid

VKH DiseaseLaboratory InvestigationsOCTUseful in monitoring resolution of exudative retinal detachmentOn presentation4 weeks after systemic corticosteroid

Слайд 31VKH Disease
May be useful in detecting early retinal damage.

Macular function

is severely impaired in patients with active uveitis.
Treatment with immunosuppressive

agents leads to delayed but limited recovery of macular function.
May be useful in guiding therapy.

Laboratory Investigations

Chee et al: Graefe’s Arch Clin Exp Ophthalmol 2005; 243:785.

Multifocal Electroretinogram

Yang et al: Am J Ophthalmol 2008; 146:767.

VKH DiseaseMay be useful in detecting early retinal damage.Macular function is severely impaired in patients with active

Слайд 32VKH Disease
Patients displayed a markedly decreased BCVA, fixation stability and

mean retinal sensitivity at baseline.
BCVA and fixation stability recovered earlier,

faster and better than mean retinal sensitivity.
At final follow-up, retinal sensitivity was significantly reduced even in eyes with full recovery of BCVA.
Subclinical macular dysfunction is a permanent damage in VKH disease.

Retinal functional changes measured by microperimetry after immunosuppressive therapy

Abu El-Asrar et al: Eur J Ophthalmol 2012; 22:368

VKH DiseasePatients displayed a markedly decreased BCVA, fixation stability and mean retinal sensitivity at baseline.BCVA and fixation

Слайд 33VKH Disease
Retinal functional changes measured by microperimetry after immunosuppressive therapy

VKH DiseaseRetinal functional changes measured by microperimetry after immunosuppressive therapy

Слайд 34VKH Disease
Lumbar Puncture:
Rarely necessary in a typical case.
CSF pleocytosis (mostly

lymphocytes).
Transient and resolves within 8 weeks.
Laboratory Investigations

VKH DiseaseLumbar Puncture:Rarely necessary in a typical case.CSF pleocytosis (mostly lymphocytes).Transient and resolves within 8 weeks.Laboratory Investigations

Слайд 35VKH Disease
Lumbar Puncture:
Frequency of CSF pleocytosis and the number of

cells in CSF at disease onset were significantly higher in

patients who eventually developed sunset glow fundus.

Laboratory Investigations

Keino et al: Am J Ophthalmol 2006; 141:1140.

VKH DiseaseLumbar Puncture:Frequency of CSF pleocytosis and the number of cells in CSF at disease onset were

Слайд 36VKH Disease
Cataract
Secondary glaucoma
Choroidal neovascular membranes
Subretinal fibrosis
Severe chorioretinal atrophy
Significantly associated with

longer duration of disease and greater numbers of recurrences.

Complications
Read et

al : Am J Ophthalmol 2001;131:599.
Sonoda et al: Jpn J Ophthalmol 1999;43:113.
VKH DiseaseCataractSecondary glaucomaChoroidal neovascular membranesSubretinal fibrosisSevere chorioretinal atrophySignificantly associated with longer duration of disease and greater numbers

Слайд 37VKH Disease
Significantly associated with older age and more severe disease

at presentation.

Complications
Al-Kharashi, Abu El-Asrar: Int Ophthalmol

2007;27:201
VKH DiseaseSignificantly associated with older age and more severe disease at presentation. Complications Al-Kharashi,

Слайд 38VKH Disease
Should be prompt and aggressive.
Systemic corticosteroids are mainstay of

therapy.
1-1.5 mg/kg/day of oral Prednisone (single morning-after-breakfast dose).
For 6-12 months

with slow gradual tapering during this time.
Hospitalization with careful follow-up.

Therapy

VKH DiseaseShould be prompt and aggressive.Systemic corticosteroids are mainstay of therapy.1-1.5 mg/kg/day of oral Prednisone (single morning-after-breakfast

Слайд 39VKH Disease
Intravenous high-dose pulse steroid therapy (1g/day of Methylprednisolone given

for 3 days) followed by oral Prednisone (1 mg/kg/day).
Topical Prednisone

1% solution and cycloplegics for anterior uveitis.
Patients adequately treated with corticosteroids have a fair visual prognosis.
Recurrences are associated with rapid or early decrease in steroid doses.

Therapy

VKH DiseaseIntravenous high-dose pulse steroid therapy (1g/day of Methylprednisolone given for 3 days) followed by oral Prednisone

Слайд 40VKH Disease
Such treatment may shorten duration of disease, prevent progression

into chronic stage, reduce incidence of extraocular manifestations.
Failure to prescribe

proper corticosteroid therapy in initial phase may lead to chronic recurrent uveitis that may result in severe visual loss due to extensive chorioretinal atrophy.

Therapy

Sonoda et al: Jpn J Ophthalmol 1999;43:113.

VKH DiseaseSuch treatment may shorten duration of disease, prevent progression into chronic stage, reduce incidence of extraocular

Слайд 41VKH Disease
Final VA of 20/20 was significantly associated with use

of systemic corticosteroids for longer than 9 months and slow

tapering.
Recurrent inflammation was significantly associated with rapid tapering of systemic corticosteroids.

Therapy

Al-Kharashi, Abu El-Asrar: Int Ophthalmol 2007;27:201

VKH DiseaseFinal VA of 20/20 was significantly associated with use of systemic corticosteroids for longer than 9

Слайд 42VKH Disease
Patients treated initially with immunomodulatory drugs (mycophenolate mofetil, cyclosporine

A, azathioprine, and methotrexate) combined with corticosteroids had a better

visual outcome than those who received corticosteroids as monotherapy.
Immunomodulatory therapy combined with corticosteroids should be considered as first-line therapy for patients with VKH.

Therapy

Paredes et al: Ocul Immunol Inflamm 2006;14:87
Kim and Yu: Ocul Immunol Inflamm 2007;15:381
Abu El-Asrar, et al: Acta Ophthalmol 2012;90:e603

VKH DiseasePatients treated initially with immunomodulatory drugs (mycophenolate mofetil, cyclosporine A, azathioprine, and methotrexate) combined with corticosteroids

Слайд 43VKH Disease
Use of mycophenolate mofetil as first-line therapy combined with

systemic corticosteroids is safe and effective in the treatment of

acute uveitis associated with VKH disease.
It has marked corticosteroid-sparing effect and significantly reduced development of chronic recurrent inflammation and late complications and significantly improved visual outcome.

The outcomes of mycophenolate mofetil combined with systemic corticosteroids in acute uveitis associated with VKH disease

Abu El-Asrar et al: Acta Ophthalmol 2012; 90:e603

VKH DiseaseUse of mycophenolate mofetil as first-line therapy combined with systemic corticosteroids is safe and effective in

Слайд 44VKH Disease
Visual prognosis is generally favorable.
87.5% achieved V.A. of ≥20/40.
High-dose

systemic corticosteroids for >9 months with slow tapering significantly improves

the prognosis and decreases risk of recurrence.
Age older than 18 years is significantly associated with the development of complications.
Visual prognosis is generally favorable in children.

Prognosis

Al-Kharashi, Abu El-Asrar: Int Ophthalmol 2007;27:201
Abu El-Asrar et al: Eye 2008;22:1124

VKH DiseaseVisual prognosis is generally favorable.87.5% achieved V.A. of ≥20/40.High-dose systemic corticosteroids for >9 months with slow

Слайд 45VKH Disease
Poor visual acuity and severe anterior segment inflammation at

presentation are significantly associated with a worse outcome.
Chronic recurrent disease

is significantly associated with more severe anterior segment inflammation and less exudative retinal detachment at presentation, more ocular complications and a worse visual outcome compared with initial-onset disease.
Use of immunomodulatory therapy as first-line therapy combined with systemic corticosteroids significantly improved clinical outcomes.

Prognostic factors for clinical outcomes in patients treated with high-dose corticosteroids

Abu El-Asrar et al: Acta Ophthalmol. In press.

VKH DiseasePoor visual acuity and severe anterior segment inflammation at presentation are significantly associated with a worse

Слайд 46Sympathetic Ophthalmia
Ahmed M. Abu El-Asrar, MD, PhD

Sympathetic OphthalmiaAhmed M. Abu El-Asrar, MD, PhD

Слайд 47Sympathetic Ophthalmia
Rare bilateral granulomatous panuveitis that occurs as a complication

of a penetrating injury that involves the uvea of one

eye.
Accidental trauma or surgery.
Injured eye is referred to as the exciting eye and fellow eye as the sympathizing eye.
Sympathetic OphthalmiaRare bilateral granulomatous panuveitis that occurs as a complication of a penetrating injury that involves the

Слайд 48Sympathetic Ophthalmia
In 0.1% to 0.3% of patients after accidental trauma.
In

0.015% of patients following ocular surgery.


5.8% and 0.67% after noncontact

and contact Nd:YAG cyclotherapy, respectively.

Incidence

Allen: JAMA 1969;209:1090
Liddy, Stuart: Can J Ophthalmol 1972;7:157
Gass: Am J Ophthalmol 1982;93:552

Lam et al: Ophthalmology 1992;99:1818

Sympathetic OphthalmiaIn 0.1% to 0.3% of patients after accidental trauma.In 0.015% of patients following ocular surgery.5.8% and

Слайд 49Sympathetic Ophthalmia
Role of ocular surgery
Sole cause in:
45% of cases (Gass:

Am J Ophthalmol 1982;93:552)
17% of cases (Hakin et al: Eye

1992;6:453)
28% of cases (Chan et al: Arch Ophthalmol 1995;113:597)
56% of cases (Kilmartin et al: Br J Ophthalmol 2000;84:259)
70% of cases (Su and Chee: Graefes’ Arch Clin Exp Ophthalmol
2006;244:243)
38% of cases (Galor et al: Am J Ophthalmol 2009;148:704)

Incidence

Sympathetic OphthalmiaRole of ocular surgerySole cause in:45% of cases (Gass: Am J Ophthalmol 1982;93:552)17% of cases (Hakin

Слайд 50Sympathetic Ophthalmia
Role of ocular surgery
Ocular surgery, particularly retinal surgery, is

now a greater risk than accidental trauma.

Risk of one in

1152 retinal surgical procedures.

Incidence

Kilmartin et al: Br J Ophthalmol 2000;84:448

Kilmartin et al: Br J Ophthalmol 2000;84:259
Su and Chee: Graefe’s Arch Clin Exp Ophthalmol 2006;244:243

Sympathetic OphthalmiaRole of ocular surgeryOcular surgery, particularly retinal surgery, is now a greater risk than accidental trauma.Risk

Слайд 51Sympathetic Ophthalmia
Role of vitrectomy
In 0.06% of cases
In 0.01% when vitrectomy

was the only operative procedure and penetrating wound.

A prospective surveillance

for SO in UK and Ireland showed risk of one in 799 vitrectomies.

Incidence

Kilmartin et al: Br J Ophthalmol 2000;84:448

Gass: Am J Ophthalmol 1982;93:552

Sympathetic OphthalmiaRole of vitrectomyIn 0.06% of casesIn 0.01% when vitrectomy was the only operative procedure and penetrating

Слайд 52Sympathetic Ophthalmia
Role of vitrectomy
Vitreoretinal surgery is an important risk factor.
It

may be appropriate to counsel patients about risk of SO

before performing vitrectomy

Any bilateral uveitis following vitreoretinal surgery should alert the surgeon to the possibility of SO.

Incidence

Kilmartin et al: Br J Ophthalmol 2000;84:448

Sympathetic OphthalmiaRole of vitrectomyVitreoretinal surgery is an important risk factor.It may be appropriate to counsel patients about

Слайд 53Sympathetic Ophthalmia
Evisceration versus enucleation
Uveal tissue may be left behind after

evisceration and act as the source of the immune response.
Controversy

involving evisceration and risk of SO.

Incidence

Sympathetic OphthalmiaEvisceration versus enucleationUveal tissue may be left behind after evisceration and act as the source of

Слайд 54Sympathetic Ophthalmia
Evisceration versus enucleation
Four cases of SO following evisceration

Six cases

of SO after evisceration.

A case of SO following evisceration of

a blind, painful, post-traumatic, glaucomatous eye.

Incidence

Green et al: Trans Am Acad Ophthalmol Otolaryngol 1972; 76:625

Ikui et al: Nippon Ganka Kiyo1965; 16:458

Griepentrog et al: Ophthal Plast Reconstr Surg 2005; 21:316

Sympathetic OphthalmiaEvisceration versus enucleationFour cases of SO following evisceration Six cases of SO after evisceration.A case of SO

Слайд 55Sympathetic Ophthalmia
Evisceration versus enucleation
Evisceration is safe with little risk of

SO.


High degree of clinical suspicion is required.
Incidence
Levine et

al: Ophthal Plast Reconstr Surg 1999; 15:4.
Toit et al: Br J Ophthalmol 2008;92:61.
Sympathetic OphthalmiaEvisceration versus enucleationEvisceration is safe with little risk of SO. High degree of clinical suspicion

Слайд 56Sympathetic Ophthalmia
Interval between injury and onset of inflammation ranges from

5 days to 66 years.
70 to 80% occur within 3

months and 90% within 1 year of injury.
Peak incidence occurs at 4 to 8 weeks following injury.

Clinical Manifestations

Lubin et al: Ophthalmology 1980;87:109
Zaharia et al: Can J Ophthalmol 1984;19:240
Manak: Surv Ophthalmol 1979;24:141

Sympathetic OphthalmiaInterval between injury and onset of inflammation ranges from 5 days to 66 years. 70 to 80%

Слайд 57Sympathetic Ophthalmia
50-year-old man.
Underwent successful retinal reattachment surgery with pars plana

vitrectomy and gas tamponade.
Developed SO 5 weeks after surgery
Treatment: I.V.

and oral steroids + cyclosporin A.
Control of inflammation and good visual prognosis.

After successful retinal reattachment surgery with vitrectomy

Sympathetic Ophthalmia50-year-old man.Underwent successful retinal reattachment surgery with pars plana vitrectomy and gas tamponade.Developed SO 5 weeks

Слайд 58Sympathetic Ophthalmia
31-year-old man.
Underwent retinal reattachment surgery with silicone oil tamponade

in his left eye 3 mos. prior to presentation.
VA: CF

OU
Treatment: I.V. and oral steroids + mycophenolate mofetil
Control of inflammation and good visual prognosis.

After retinal reattachment surgery with silicone oil tamponade

Sympathetic Ophthalmia31-year-old man.Underwent retinal reattachment surgery with silicone oil tamponade in his left eye 3 mos. prior

Слайд 59Sympathetic Ophthalmia
50-year-old man.
Developed SO 8 weeks after cataract surgery.
Treatment: Oral

steroids + cyclosporin A + pars plana vitrectomy and removal

of IOL.
Control of inflammation and good visual prognosis.

After complicated cataract surgery and IOL implantation

Sympathetic Ophthalmia50-year-old man.Developed SO 8 weeks after cataract surgery.Treatment: Oral steroids + cyclosporin A + pars plana

Слайд 60Sympathetic Ophthalmia
28-year-old man.
Developed SO 12 weeks after sustaining penetrating trauma.
Treatment:

Oral steroids + cyclosporin A.
Control of inflammation and good visual

outcome.

After penetrating trauma

Sympathetic Ophthalmia28-year-old man.Developed SO 12 weeks after sustaining penetrating trauma.Treatment: Oral steroids + cyclosporin A.Control of inflammation

Слайд 6138-year-old lady.
Lt. eye blind since childhood with no known clear

cause.
Developed SO 9 weeks after left eye cyclophotocoagulation that was

done prior to referral.

Sympathetic Ophthalmia

After cyclophotocoagulation

38-year-old lady.Lt. eye blind since childhood with no known clear cause.Developed SO 9 weeks after left eye

Слайд 62Sympathetic Ophthalmia
After cyclophotocoagulation

Sympathetic OphthalmiaAfter cyclophotocoagulation

Слайд 63Sympathetic Ophthalmia
Vogt-Koyanagi-Harada disease

(No previous ocular trauma or surgery)
Differential Diagnosis

Sympathetic OphthalmiaVogt-Koyanagi-Harada disease(No previous ocular trauma or surgery)Differential Diagnosis

Слайд 64Sympathetic Ophthalmia
Immunogenetics
Genetics predisposition which is very similar to VKH disease.
Increased

frequency of HLA-A11 antigen in patients with SO.

Associated with HLA-DRB1*04,

DQA1*03, DQB1*04 among Japanese, British, Irish patients.

Pathogenesis

Reynard et al: Am J Ophthalmol 1983;95:216

Shindo et al; Tissue Antigens 1997;49:111
Kilmartin et al: Br J Ophthalmol 2001;85:281.

Sympathetic OphthalmiaImmunogeneticsGenetics predisposition which is very similar to VKH disease.Increased frequency of HLA-A11 antigen in patients with

Слайд 65Sympathetic Ophthalmia
Similar in both exciting and sympathizing eyes.
Classic description is

that of a diffuse non-necrotizing granulomatous choroidal inflammation with Dalen-Fuchs

nodules.
Relative sparing of the choriocapillaris or retina (uncharacteristic feature).

Pathological Features

Sympathetic OphthalmiaSimilar in both exciting and sympathizing eyes.Classic description is that of a diffuse non-necrotizing granulomatous choroidal

Слайд 66Sympathetic Ophthalmia
Prevention
Careful microsurgical management of the wound with prompt closure

of all penetrating injuries.

Management

Sympathetic OphthalmiaPreventionCareful microsurgical management of the wound with prompt closure of all penetrating injuries.Management

Слайд 67Sympathetic Ophthalmia
Prevention
Enucleation of the traumatized eye if unsalvageable by modern

surgical methods within two weeks after injury is the only

known preventive way.
Problems:
No proof that this is actually of value.
Incidence of SO after penetrating injury is decreasing.
With current advanced surgical techniques many eyes may have a fair prognosis.

Management

Sympathetic OphthalmiaPreventionEnucleation of the traumatized eye if unsalvageable by modern surgical methods within two weeks after injury

Слайд 68Sympathetic Ophthalmia
Controversy regarding any advantage of enucleating the exciting eye

once SO has started in the sympathizing eye.
Management

Sympathetic OphthalmiaControversy regarding any advantage of enucleating the exciting eye once SO has started in the sympathizing

Слайд 69Sympathetic Ophthalmia
Enucleation within 2 weeks of onset is associated with

a relatively benign clinical course and improves visual outcome.

Enucleation is

valueless and should not be performed.
Enucleation of the exciting eye did not result in improved visual function in the sympathizing eye.

Management

Winter: Am J Ophthalmol 1955;39:340

Lubin et al: Ophthalmology 1980;87:109
Reynard et al: Am J Ophthalmol 1983;96:290

Sympathetic OphthalmiaEnucleation within 2 weeks of onset is associated with a relatively benign clinical course and improves

Слайд 70Sympathetic Ophthalmia
Exciting eye may eventually have the better vision, or

diagnosis may be incorrect.

Enucleation should be considered only in eyes

with nil visual prognosis.

Management

Sympathetic OphthalmiaExciting eye may eventually have the better vision, or diagnosis may be incorrect.Enucleation should be considered

Слайд 71Sympathetic Ophthalmia
It is not justified to remove a functionally useful

injured eye in established cases of SO for the purpose

of decreasing inflammation.

Not all inciting eyes are “lost eyes” as commonly believed.

Management

Sympathetic OphthalmiaIt is not justified to remove a functionally useful injured eye in established cases of SO

Слайд 72Sympathetic Ophthalmia
Early diagnosis.
Prompt and effective treatment with systemic immunosuppressive agents

has improved the prognosis.
Management

Sympathetic OphthalmiaEarly diagnosis.Prompt and effective treatment with systemic immunosuppressive agents has improved the prognosis.Management

Слайд 73Sympathetic Ophthalmia
Corticosteroids are the mainstay of treatment.
I.V. pulses, I g/day

methylprednisolone, 3 consecutive days for immediate control

of inflammation.
Followed by oral prednisone 1-1.5 mg/ Kg/day.
Dose is reduced gradually following clinical resolution of uveitis.
Continued for at least 6 months.

Management

Sympathetic OphthalmiaCorticosteroids are the mainstay of treatment.I.V. pulses, I g/day methylprednisolone, 3 consecutive days

Слайд 74Sympathetic Ophthalmia
Successful control of inflammation and good visual prognosis

is related to prompt and adequate systemic immunosuppression using combination

of systemic steroids and steroid sparing agents such as cyclosporin A, azathioprine, mycophenolate mofetil.

Management

- Hakin et al: Eye 1992;6:453
Chang et al: Arch Ophthalmol 1995;113:597
Kilmartin et al: Br J Ophthalmol 2000;84:259
Abu El-Asrar, Al-Obeidan: Eur J Ophthalmol 2001;11:193

Sympathetic OphthalmiaSuccessful control of inflammation and good visual prognosis is related to prompt and adequate systemic

Слайд 75Sympathetic Ophthalmia
Rare disease.
Major sight-threatening disorder.
High index of suspicion must be

maintained whenever inflammation occurs in fellow eyes of an eye

that has suffered penetrating trauma or intraocular surgery.
Infection should be carefully ruled out.

Conclusions

Sympathetic OphthalmiaRare disease.Major sight-threatening disorder.High index of suspicion must be maintained whenever inflammation occurs in fellow eyes

Слайд 76Sympathetic Ophthalmia
Diagnosis is made clinically, histological proof is not required.
Injured

eyes which have potential vision should not be enucleated in

an attempt to prevent or lessen SO or to provide confirmatory pathology.

Conclusions

Sympathetic OphthalmiaDiagnosis is made clinically, histological proof is not required.Injured eyes which have potential vision should not

Слайд 77Sympathetic Ophthalmia
Prognosis was considered poor prior to the use of

systemic immunosuppression.
Today, it should no longer be regarded as a

blinding disease.
Prompt and adequate systemic immunosuppressive therapy with systemic steroids and steroid-sparing agents has improved prognosis.

Conclusions

Sympathetic OphthalmiaPrognosis was considered poor prior to the use of systemic immunosuppression.Today, it should no longer be

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