Lecture on Sympathetic Ophthalmia For 4th Year MBBS Undergraduate Students By Prof. Dr. Hussain Ahmad Khaqan

1. Sympathetic Ophthalmia
Prof. Dr. Hussain Ahmad Khaqan
 MD
 FRCS(Glasgow)
 FCPS(Ophth.)
 FCPS(Vitreo Retina)
 MHPE (KMU)
 CICO(UK)
 CMT(UOL)
 Fellowship in Medical Retina (LMU, Munich)
 Fellowship in Vitreo Retinal Surgery (LMU, Munich)
 Consultant Ophthalmologist & Retinal Surgeon
Professor of Ophthalmology
Lahore General Hospital, Lahore
Ameer Ud Din Medical College, Lahore
Post Graduate Medical Institute, Lahore
Shaukat Khanum Memorial Cancer Hospital & Research Centre ,Lahore

2. DEFINITION
• Sympathetic ophthalmia is a rare bilateral
granulomatous panuveitis related to antecedent
trauma or surgery. Although this response to injury
can occur within a few days or over 60y later, it
usually arises between 1 and 12mo after injury. It
appears to be a T-cell-mediated response to an
ocular antigen, presumably liberated during the
initial insult.

3. SYMPTOMS
• Bilateral eye pain
• Photophobia
• Decreased vision (near vision is often affected
before distance vision)
• Red eye
• History of penetrating trauma or intraocular surgery.

4. SIGNS
• Anterior: bilateral granulomatous anterior uveitis
with mutton fat KPs (keratic precipitates), PS
(posterior synechiae)
• Posterior: vitritis, choroidal infiltration, dalen–Fuchs
nodules, macular oedema, ERD (exudative retinal
detachment); the exciting eye may be phthisical.
• Complications: cataract, secondary glaucoma, end-
stage disease (optic atrophy, chorioretinal scarring).

5. Figure: Mutton fat keratic precipitates. Figure: Posterior synechiae.
Figure: Dalen-Fuchs nodulesFigure: Optic disc atrophy.

6. DIFFERENTIAL DIAGNOSISvcontinue
• VKH (Vogt-Koyanagi-harada) syndrome: Similar
signs, but no history of ocular trauma or surgery.
Other systemic symptoms.
• Phacoanaphylactic endophthalmitis: Severe anterior
chamber reaction from injury to the lens capsule.
Contralateral eye is uninvolved.
• Sarcoidosis: Often elevated ACE (angiotensin
converting enzyme) level. May cause a bilateral
granulomatous panuveitis.

7. • Syphilis: Positive FTA-ABS (Fluorescent treponemal
antibody absorption test) or treponemal-specific
assay. May cause bilateral granulomatous panuveitis.
• Tuberculosis: Positive PPD (purified protein
derivative) and CXR (chest x-ray) or chest CT. May
cause bilateral granulomatous panuveitis.
• Multifocal choroiditis with panuveitis: Usually
bilateral, with no history of trauma.
DIFFERENTIAL DIAGNOSIS

8. WORK-UP
• History: Any prior eye surgery or injury? Venereal disease?
Difficulty breathing?
• Complete ophthalmic examination, including a dilated retinal
examination.
• Assess for any systemic findings to rule out VKH (Vogt-
Koyanagi-harada) (e.g., neurologic, skin, or auditory changes).
• CBC (complete blood count), RPR (rapid plasma reagin) or
VDRL (venereal disease research laboratory),FTA-ABS
(Fluorescent treponemal antibody absorption test), or
treponemal-specific assay.
• Chest radiograph or CT to evaluate for tuberculosis or
sarcoidosis.
• IVFA (intravenous fluorescein angiography) or B-scan
ultrasound, or both, to help confirm the diagnosis.

9. TREATMENT continue
• Prevention: Enucleation of a blind, traumatized eye
before a sympathetic reaction can develop (usually
considered within 14 days of the trauma). Once
sympathetic ophthalmia develops, enucleation of the
sympathizing eye appears to have no benefit.
• Topical steroids (e.g. prednisolone acetate 1% q1–2h
or difluprednate 0.05% q2h). Topical steroids are
tapered slowly as condition improves.
• Periocular or intravitreal steroids (e.g., subconjunctival
triamcinolone acetate 40 mg in 1 mL).
• Systemic steroids (e.g., prednisone 60 to 80 mg p.o.
daily) with calcium/vitamin D supplementation and
antiulcer prophylaxis.

10. • Slow-release intravitreal steroid implants (e.g.,
dexamethasone 0.7 mg intravitreal implant;
fluocinolone acetonide 0.19 or 0.59 mg intravitreal
implant) are alternatives to oral steroids.
• Cycloplegic (e.g., atropine 1% b.i.d.).
• Long-term systemic immunosuppression with
corticosteroid-sparing agents is essential in most
cases. Choice of immune suppression should be
made in conjunction with a uveitis specialist and
individualized for each patient.
TREATMENT