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Ocular Manifestations of Inflammatory Bowel Disease
- 1. Ocular Manifestations of Inflammatory Bowel Disease Raed Behbehani , MD FRCSC
- 2. Burrill Bernard Crohn • Reported two cases with UC who severe pain and photophobia and peripheral corneal ulcerations . • Crohn, B. B. (1925). Ocular lesions complicating ulcerative colitis. Amer. J. med. Sci., 169, 260-267.
- 3. Etiology of IBD • Multiple etiologic factors. • Genetic (Nod2 gene on chromosome 16) • Infectious • Immunological dysregulation (increased TNF- alpha and IFN gamma)
- 4. Extra-Intestinal Manifestations • Skin , Eye , Joints , Hepato-biliary system. • Ocular manifestations occur in 4-10% of patients. • conjunctivitis, episcleritis, scleritis, marginal keratitis, anterior uveitis, retinitis, retinal vascular occlusive disease, optic neuritis, and orbital inflammatory disease
- 5. Ocular Manifestations • Risk is higher in patients with colitis and ileocolitis than ileitis. • Patient with Arthritis have 33% risk for ocular involvement. • 50% have more than one ocular complication and 68% of patients with ophthalmic complications may also have at least one other extraintestinal manifestation.
- 6. Pathophysiology of Ocular Involvement • Circulating antigen-antibody complexe. • Autoantibody production against cellular antigens. • Damage to GI mucosa allows leakage of proteins and microorganisms—> reactive lymphoid hyerplasia —> Antigen-Antibody complex —> Systemic involvement. • Higher prevalence of HLA-B27.
- 7. Episcleritis • The most common ocular manifestation in IBD. • Nodular , diffuse • Injection (sectoral or diffuse) • Blanches with topical application of phenylephrine.
- 8. Episcleritis • Vessels can be moved with a cotton tip applicator. • Pain is mild to moderate. • In CD can indicate disease activity .
- 10. Episcleritis Treatment • Mild-Idiopathic : Tear drops , topical NSAID • Moderate-Severe : Systemic NSAID , topical steroids • Must treat underlying disease (anti-TNF e.g, Infliximab)
- 11. Scleritis • Less common in IBD. • Deep more sever pain. • More morbidity. • 50% have an underlying systemic disease • Needs more aggressive treatment.
- 12. Scleritis • Anterior - Posterior • Nodular- Diffuse • Necrotizing-Nonnecrtozing
- 13. Scleritis • Recurrent scleritis can lead to scleromalacia.
- 14. Scleritis Treatment • NSAID. • Steroids. • Immunosuppressive agents (azathioprine, mycophenolate mofetil, cyclophosphamide, or cyclosporine) • Anti-TNF (infliximab or adalimumab)
- 15. Anterior Uveitis • Uveitis (Anterior, intermediate , posterior) • Pain , photophobia. • Association between CD, and sacroiliitis. • HLA-B27
- 16. Uveitis • Low grade non- granulomatous iritis. • Insidious and may persist up to 6 months. • 60% recurrent anterior uveitis . • 10% non-recurrent anterior uveitis. • 30% panuveitis. (choroiditis)
- 17. Uveitis , Scleritis , Episcleritis
- 18. Optic Neuritis in IBD
- 19. Neuro-ophthalmic Manifestations • Associated with iritis, vitritis,retinal vas- culitis, and choroiditis. • Optic neuropathy secondary to dietary deficiency . • Vasocclusive complications (Hemiparesis , gaze palsy, Hemianopia)
- 20. Keratitis • Sub-epithelial keratitis • Small subepithelial corneal infiltrates. • Bilateral and symmetric.
- 21. Orbital Complications • 1% cases of proptosis. • Orbital inflammatory syndrome , orbital myositis. • Responds to steroids. • Must differentiate from Orbital Cellulitis.
- 22. Retinal Complications • Rare • Retinal vascular occlusion , retinal edema and serous detachments of the retina. • Retinal arteriolar and vein occlusion. • Cystoid macular edema (20%) in posterior uveitis.
- 26. Management • Topical steroids. • Periocualr steroids. • Systemic steroids , NSAID. • Cytotoxic immunosuppressive. • Monoclonal antibody (anti-tTNF) e.g. adalimumab, infliximab
- 28. Glaucoma Treatment • Medical : Topical Beta-blockers (Timolol) , Alpha- agonists (Brimonidne) , Prostaglandin analogues. • Surgical : Laser for acute angle closer glaucoma , Filtering surgery (trabeculectomy, Glaucoma drainage device) , Ciliary body ablation.
- 29. Trabeculectomy
- 32. Other Ocular Complications • Endogenous endophthalmitis (central line) • Nutritional Optic neuropathy and retinopathy , Wernicke’s Encephalopathy (B12, thiamine deficiency) • Cyclosporine in Crohn’s disease ( optic neuropathy, ophthalmoplegia, and nystagmus).
- 33. Anti-TNF alpha and Risk of Optic Neuritis • Anti-TNF alpha associated with demyelination. • 17 cases reported in literature. • Large cohort study (SABER) incidence of ON 5–5-10 per 100,000 patient-years. • Not different from non-biologic disease modifying drugs. • In patients with underlying demyelinating disease , anti-TNF alpha should be avoided.
- 34. Summary • Episcleritis , scleritis and anterior uveitis are the most common eye manifestation of IBD. • Ocular manifestations are common in patients with colitis and other extra-GI manifestation. • Treatment of underlying IBD is often effective. • Steroids , immunuppressives and anti-TNF agents are used in resistant cases. • Cataract and glaucoma are sequelae of uveitis in IBD.
Editor's Notes
- You would be surprised to know that the first report of the ocular complications of IBD were made by Doctor Crohn himself.. who reported …
- The etiology of IBD is still not well-defined .. Nod2 gene mutation has been implicated.. Microbiological agents And Immune dyregulation (increased TNF alpha and IFN gamma)
- Ocular manifestations are very uncommon in IBD compared to possibly other extra-GIT sites. By enlarge the most common ocular complications are episclritis , scleritis , and AU ..
- For some reason patients who have colitis, arthritis and other extra intestinal manifestations such as dermatologic , rather than ileitis alone are at a greater risk for ocular complications , 50 % Patients can develop more than one complications for example a patient can have as uveitis and scleritis for example..
- Why do ocular complications occur ? various theories … Damage to GI mucosa may explain why patients with colonic involvement, which is more rich in bacateria and micro-organisms , have a higher prevalence of ocular complications. (colonic antigens—> immune response —> inflammation). Finally , patients with eye involvement and Crohn’s disease have a higher prevalence of HLA-B27, who are at a higher risk for uveitis anyway.
- Because it will look like scleritis , one way to tell is applying topical phenyelperine , which will readily constrict the superficial episcleral vessels but not the deep scleral vessels.
- Another way to differentiate epi-scleritis from scleritis is using cotton tip applicator .. In CD , episcleritis has been used to indicate disease activity.
- This is an example of diffuse vs nodular episcleritis
- Treating the underlying cause , in the case of IBD , using anti-TNF such as infliximab has been shown to be effective.
- Scleritis , however…. 50% of patients who present to the ophthalmologist with scleritis will have un underlying systemic disease , usually vasculitis or some type of systemic vasculitis or rheumatologic disease such as RA , SLE , or gnaulmatous angitis (WG) .
- There are different ways of classifying scleritis ..
- This what happens with recurrent necrotizing scleritis , loss of sclera leading to exposure of the underlying uvea in the eye.
- Since scleritis is associated with greater morbidity , treatment has to be aggressive. For mild nocular or diffuse scleritis , NSAID can be started first and if no response is seen than systemic steroids , or immunosuppressive agents can be used. Anti-TNF can be used if previous therapy fails.
- In clinical practice this will be the most common complications since episclerits tends to be self-limiting and patients do not seek treatment. Patients with AU will present with pain , and photophobia .
- The AU tends to be …..low-garde and indidious . Many patients with experience recurrences even after successful treatment . Although in the majority , AU tends to be anterior (involves iris and ciliary body) , in 30% it can involve the posterior eye (the choroid and the retina),
- Extremely rare ! In fact I found one report in whole literature and even then it is not clear whether ON was due to ON or something else .
- Tend to occur with panuveitis with involvement of the retina and choroid. Because patients with IBD can have nutritional deficiencies such as vitamin A , B , this can affect optic nerve functions. Patients who develop strokes (because of vasculitis ) can develop other neuro-ophthalmic features such has gaze palsy and visual field defects.
- SEI : (0.3 to 0.5 mm), irregular, round or oval, white nodular , 2 to 3 mm inside the cornea. These can cause blurred vision and photosensitivity and are usually treated with topical steroids.
- It is important here to differentiate this from an infectiousorbital cellulitis , which is a serious condition that requires prompt treatment with IV antibiotics.
- Retinal complications are very uncommon .
- This retinal vasculits in a patient with IBD . You can notices the sheathing (candle wax dripping) of vessels and some hemorrhages and area of whitening and retintis . You will see staining with flourescin.
- CME (which is fluid in the macula) is an important cause of decreased vision in patients with uveitis . We have have very good ways of diagnosing this condition with either OCT (on the left) or IV fluorescing angiography (on the right).
- This is a patient with Crohn’s disease and CSR. CSR is basically fluid in the retina due to disruption o the retina-blood barrier (tight-junctions in the RPE) serves this barrier and for some reason this is disrupted as in inflammation or secondary to systemic steroids. (Top left) fundus image shows blister (bottom left) IVF shows the pin-point area leakage of fluid causing this blister (bottom right) OCT appearance and the dark areas (hyporelfective) shows the area of the sub-retinal fluid.
- Step-wise manner . Steroids are still the mainstay of therapy. Steroids sparing agents : anti-metabolites (MTX , Azathioprine , Mycophenolic acid) or alkylating agents (cyclophosphamide) if steroids fail or to reduce the dose of steroids. (Anti-TNF) use in uveitis is based on uncontrolled trials or retrospective studies and have investigated cases of uveitis refractory to immunosuppression. Anti-TNF treatment has had success in JIA , Behcet’s disease and Sarcoidosis uveitis. Due to lack of evidence thus far, the biologics are reserved for such refractory cases or if occurring in patients with other systemic symptoms that would normally be treated with biologics.
- Chronic eye inflammation will give rise to many ocular complications but the most important are glaucoma and cataract. Glaucoma in uveitis can be either acute (proteins, inflammatory cells and debris ) of chronic due to inflammation ( cytokines and PG-mediated inflammation) and scaring of the TM. In addition , Steroids (topical, systemic) raise IOP and thus patients require monitoring.
- Cataracts can arise from inflammation or steroids. Often more complicated and require special planing in order to control the inflammation ahead of surgery and post-operatively . Higher rate of surgical complications such as inflammation and generally more technically difficult cases , in addition to post-operative glaucoma and cystoid macular edema .
- Other complications you may need to remember that .. Patient who require central line can develop endogenous endophthalmitis (fungal). Because these patients can have nutritional deficiencies (B1, B12) they can also develop nutritional optic neuropathy or retinopathy. Some of the drugs given for IBD are neurotoxic such as cyclosporine ( optic neuropathy ) and IFN-alpha (retinopathy) , which we see in patients with HVC taking IFN for treatment.
- Anti-TNF alpha agents have been associated with optic neuritis. There are about 17.. A large cohort looked at this and found that the incidence is not much different from non-biologic drugs . However, it is probably prudent to avoid the use of anti-TNF alpha in patients with demyelinating disease.