You are on page 1of 23

Atopic Keratoconjunctivitis

Austin Strohbehn, M3; Matthew Ward, MD; Anna Kitzmann, MD
March 8, 2013
Chief Complaint: Poor vision and severe ocular itching.
History of Present Illness: A 52-year-old Caucasian male presents to the cornea clinic with a
chief complaint of vision loss. In addition to his vision loss, he complains of itchy eyes and
mucoid discharge. He also reports a history of waxing and waning eczema over the past decade.
Two years prior to this visit, he presented with similar symptoms and was treated with
medroxyprogesterone and fluoromethalone (FML) three times a day in both eyes. This medical
regimen improved his symptoms. Unfortunately, the patient discontinued his ocular prescription
and was lost to follow-up after the initial visit.
Past Ocular History: Unremarkable for surgery or trauma.
Medical History: History of uncontrolled eczema for the past decade.
Medications: He uses artificial tears as needed. Otherwise, he takes no medications or other eye
drops.
Family History: Father with cataract. No other pertinent family history.
Social History: The patient is a habitual smoker (1 pack per day).

Ocular Examination:

Visual Acuity, with correction:
o Right eye (OD): 20/60-1
o Left eye (OS): 20/70-1

Extraocular motility: Full, both eyes (OU)

Pupils: Briskly constrict from 5mm in dark to 3mm in light. No relative afferent
pupillary defect.

Confrontation Visual Fields: Full OU.

Intraocular pressure: OD — 13 mmHg; OS — 12 mmHg

Slit lamp examination:
o Lids: Hypertrophy, hyperpigmentation, and erythema of the lid skin. Cicatricial
ectropion of the lower lid. Near entire lower lid madarosis with rolled scarred lid
margin (figures 1C and D).
o Conjunctiva/sclera: Fornix foreshortening and symblepharon of the conjunctiva
with 2+ diffuse injection, more prominently OD (figure 1E).
o Cornea: Near complete conjunctivalization of the cornea with haze entering the
visual axis inferonasally (figures 1C and D).
o Anterior chamber: Deep and quiet.
o Iris: Normal
o Lens: 2+ nuclear sclerosis and 2+ posterior subcapsular cataract OU (figure 1F).

Dilated Fundus Exam:
o Hazy view to posterior pole due to conjunctivalization and posterior subcapsular
cataract, but appears normal OU.

Figure 1. Clinical signs of atopic keratoconjunctivitis.
A and B: Right and left eyes, respectively, in 2010 with periocular eczema and corneal haze. C
and D: Right and left eyes, respectively, in 2012 with progression of the disease; dense pannus
entering visual axis. E: symblepharon. F: posterior subcapsular cataract, which can be associated
with atopic keratoconjunctivitis.

and madarosis. However. his disease progressed at a rapid rate over the next two years. symblepharon. bilateral disease that relapses and remits with little to no seasonal correlation (as opposed to vernal keratoconjunctivitis). Atopic dermatitis is present in 95% of cases and asthma in 87% of cases. Conjunctivitis of the palpebral.[1] It is a chronic.[1] The primary symptom is ocular itching. and limbal . his condition was moderately severe (figures 1A and B). Unfortunately. He was treated with low potency topical corticosteroids (FML and medroxyprogesterone) which resulted in improvement in his symptoms. and his visual acuity had significantly decreased (figures 1C and D). Discussion Atopic keratoconjunctivitis (AKC) is a chronic inflammatory disease of the eye that occurs predominately between the late teenage years and the fifth decade of life. Mucoid discharge and tearing are other common symptoms. Lid manifestations include hypertrophy. he discontinued these medications sometime after he was lost to follow up. pannus. On exam at this time. the conjunctiva had entered the visual axis.Course The symptoms of itching and findings of chronic conjunctivitis. crusting.[2] Incidence of AKC increases with a family history of atopic disease. eczema. At the patient’s initial visit two years prior. His symptoms became severe enough that he decided to return for an examination. ectropion. bulbar. Periocular eczema is almost always present. cicatrization. and posterior subcapsular cataract are consistent with a diagnosis of atopic keratoconjunctivitis.

These are also useful for dermatologic manifestations of the disease. and oral anti-histamines may keep the ocular disease under control. which can permanently scar the corneal stroma and/or lead to corneal perforation. However. the Boston keratoprosthesis may be used for visual rehabilitation in motivated patients. Th2 T-cells. cold compresses. In early disease.4] When topical treatments fail to induce remission. Diagnosis: Atopic Keratoconjunctivitis . adhesion of the palpebral conjunctiva to the bulbar conjunctiva. Treatment Management of atopic keratoconjunctivitis is aimed at decreasing the inflammatory response and controlling symptoms. the diagnosis of AKC is made clinically. The pathogenesis of atopic keratoconjunctivitis has not been fully elucidated. In the final stages of atopic keratoconjunctivitis where visual loss has occurred due to corneal opacification from stem cell deficiency.[2. oral prednisone.[1] This helps aid in the diagnosis. the disease originates from a disorder of the adaptive immune system in predisposed individuals. The majority of cases are co-managed with an allergist or dermatologist to provide guidance and follow up of systemic therapy. Bulbar conjunctivitis includes hypertrophy of conjunctiva with excess mucous.[5] It is important to note that as T-cells play a central role in the pathogenesis of this disease. based on both a history of atopy and the ocular examination. Palpebral conjunctivitis is characterized by micropapillae of the tarsal conjunctiva – primarily of the lower eyelid. calcineurin inhibitors such as tacrolimus and cyclosporine are an effective route for steroid-sparing therapy in both topical and systemic applications. An admixture of mast cells. Symblepharon. or cyclosporine are the next treatment options. tacrolimus. additional pharmacologic therapy is necessary. and eosinophils is present on biopsy of the conjunctival epithelium. However. in more advanced cases. Posterior subcapsular cataracts are also common in these patients.[3] Corneal neovascularization related to stem cell deficiency occurs in approximately 60% of cases. lubricants. Th1 T-cells. conservative management with combination topical mast cell stabilizers and anti-histamine drops. [3] Corneal ulcers and erosions are more common due to the poor epithelial adhesion and predispose to infectious keratitis. In simple terms. occurs in approximately 20% of cases. or tacrolimus ointment to the eyelid skin. Pharmacologic therapy for these cases includes topical corticosteroid drops.conjunctiva is present in varying degrees. cyclosporine drops.

bilateral conjunctivitis  Males > Females  Always associated with another atopic diseas independent of its severity  Predominately presents between the late teenage years and the fifth decade of life[1] o Atopic dermatitis  Spontaneous resolution in elderly o Asthma  Associated with atopic dermatitis in 95% of cases[2] o Rhinitis  Associated with asthma in 87% of cases[2] Periocular  Eczema Lids  Blepharitis  Hypertrophy  Crusting  Cicatrization  Ectropion  Madarosis Conjunctiva  Hypertrophy of entire conjunctiva  Palpebral conjunctiva micropapillae  Hyperemia  Excessive mucous  Symblepharon in severe disease .Epidemiology Signs  <1-8% of the adult population[1]  Chronic.

03% ointment to the eye .05% eye drops  Topical tacrolimus 0.05%) for rel Advanced disease treatment  Topical cyclosporine A 0. azelastine 0. Early disease treatment  Cold compresses  Preservative free drops  Mast cell stabilizer/antihistamine (i.1%)  Antihistamine: (e.e.g. olopata or lodoxamide 0.Cornea  Erosions  Pannus  Anterior stromal scarring  Corneal thinning  Neovascularization  Perforation  Shield ulcers Lens  Symptoms  Ocular itching  Mucoid discharge  Photophobia  Decreased visual acuity  Tearing Anterior and/or posterior subcapsular catarac Treatment Therapy is aimed at treating both the ocular and the s disease.

and Ramaesh K. Topical calcineurin inhibitors in the treatment of steroid-dependent atopic keratoconjunctivitis. European Journal of Ophthalmology 2010. Atopic keratoconjunctivitis and atopic dermatitis. Atopic dermatitis and keratoconjunctivitis. Ophthalmology 1998. Tugal-Tutkun I. 5. 3. Cornea 2012. Current Opinion in Allergy and Clinical Immunology 2010. Immunology and Allergy Clinics of North America 2010. Topical corticosteroid  Consultation with allergist and/or dermatolog  Oral cyclosporine. and Akpek EK. 30(3): 323-336. tacrolimus. Guglielmetti S. Long-term follow-up of patients with atopic keratoconjunctivitis. 20(5): 844-851. Stern ME. 2. Dart JKG and Calder V. 10: 478-485. Tzu JH. or corticostero  Boston keratoprosthesis (if visual loss from c opacification has occurred) Differential Diagnoses:  Vernal keratoconjunctivitis  Seasonal allergic conjunctivitis  Perennial allergic conjunctivitis  Giant papillary conjunctivitis  Phlyctenular keratoconjunctivitis  Toxic conjunctivitis References 1. 4. Gregory ME. and Foster CS. Bielory B and Bielory L. 31(6): 649-654. Cornish KS. . Systemic cyclosporine A in severe atopic keratoconjunctivitis. Power WJ. 105(4): 637-642. Utine CA.

Ward M.htm Atopik Keratoconjunctivitis Diulas oleh Jill E.EyeRounds. March 8.kellogg. MD . EyeRounds. Kitzmann A.umich. Pada halaman ini:  Apa atopik Keratoconjunctivitis?  Gejala  Penyebab  Faktor Risiko  Tes dan Diagnosis  Pengobatan dan Obat  Klinik Informasi Apa atopik Keratoconjunctivitis? .org/cases/167-atopickeratoconjunctivitis.. Bixler. available from: http://www. Atopic Keratoconjunctivitis.org./atopic-keratoconjunct.Suggested Citation Format: Strobehn A..mei 2008 www.edu/. 2013.

Penyebab AKC adalah kondisi genetik. konjungtiva lapisan kelopak mata biasanya merah dan bengkak. jika Anda mengalami satu atau lebih gejala-gejala tersebut. dan vaskularisasi kornea. jaringan parut. Dengan AKC. katarak. Gejala  Sensitivitas terhadap cahaya  Gatal  Membakar  Merobek  Kelopak mata merah dan mengeras Gejala-gejala yang dijelaskan di atas mungkin tidak berarti bahwa Anda memiliki keratokonjungtivitis atopik. Semakin rendah kelopak mata umumnya mempengaruhi lebih dari kelopak mata atas. Meskipun AKC adalah abadi (sepanjang tahun) penyakit. Ini adalah gejala membedakan dari keratokonjungtivitis vernal mana kelopak mata atas yang paling sering terkena. hubungi dokter mata Anda untuk ujian lengkap. Tidak seperti dermatitis atopik. AKC dapat berkembang menjadi ulserasi. yang umumnya terlihat di awal masa kanak-kanak. Pria lebih sering terkena daripada wanita. Jika tidak diobati. Faktor Risiko  Riwayat keluarga beberapa alergi  Dermatitis atopik  Eksim  Asma . keratoconus. keratokonjungtivitis atopik muncul selama masa remaja akhir dan dewasa awal.Atopic keratoconjunctivitis (AKC) adalah hasil dari suatu kondisi yang disebut "atopi". gejala Anda mungkin memburuk di musim dingin. Namun. Atopi adalah kondisi genetik di mana sistem kekebalan tubuh menghasilkan antibodi lebih tinggi dari biasanya dalam menanggapi alergen tertentu.

uptodate. keratokonjungtivitis atopik (AKC). meskipun biopsi konjungtiva dapat membantu dalam membedakan AKC dari kondisi lain. Kedua jenis relatif jarang dari penyakit mata alergi dapat menyebabkan kerusakan parah pada permukaan mata. keratokonjungtivitis vernal (VKC). Dalam kasus yang lebih parah. ada potensi untuk kerusakan mata yang disebabkan oleh goresan dan menggosok. Pengobatan sistemik dari kondisi yang menyertai AKC mungkin akan sangat membantu. dan parah peradangan alergi mempengaruhi permukaan mata. bilateral. abadi konjungtivitis alergi (PAC). http://www. yang menyebabkan jaringan parut kornea dan kehilangan penglihatan jika tidak ditangani dengan baik. Hanya dalam kasus yang parah harus topikal terapi steroid dipertimbangkan. VKC dan AKC adalah bentuk kronis. Kompres dingin dan irigasi saline untuk menurunkan pH air mata tinggi juga dapat membantu. Agen steroid-sparing lain dapat membantu. Seorang dokter spesialis mata mungkin menyarankan Anda untuk memakai sarung tangan katun pada malam hari untuk mencegah kerusakan yang tidak disengaja pada permukaan okular. Pengobatan dan Obat Kombinasi antihistamin oral dan topikal dan stabilisator sel mast biasanya efektif dalam mengendalikan gejala. termasuk siklosporin atau tacrolimus. . dan konjungtivitis papiler raksasa (GPC).com/contents/atopic-keratoconjunctivitis PENDAHULUAN Ada lima jenis utama dari alergi okular: konjungtivitis alergi musiman (SAC).Tes dan Diagnosis AKC biasanya didiagnosis dengan pemeriksaan klinis dan riwayat medis dan keluarga.

4 persen dari 1. Namun. AKC ditinjau dalam topik ini. MD.) Musiman dan abadi konjungtivitis alergi. MD. and Roy S.Jenis reaksi hipersensitivitas I penting dalam penyakit ini. Studi lain menunjukkan bahwa 77 persen dari pasien dengan dermatitis atopik (AD) menderita AKC [ 4 ]. juga dibahas secara terpisah.079 pasien dengan alergi okular memiliki AKC dalam satu studi [ 3 ]. PHD .) GPC adalah gangguan inflamasi yang merupakan reaksi terhadap gerakan tutup lebih zat asing. sebagian besar karena pengawet. AKC pada umumnya mengacu pada "abadi" bentuk konjungtivitis alergi (AC) yang juga memiliki potensi keterlibatan kornea yang signifikan.cfm?RenderForPrint=1& Ophthalmic Pearls: External Disease The Itchy Eye: Diagnosis and Management of Ocular Pruritus By Jocelyn Kuryan. Yang tepat prevalensi tidak diketahui. seperti lensa kontak. Chuck. AKC Istilah ini tidak ideal. meskipun mereka bukan satu-satunya mekanisme patofisiologis.aao. (Lihat "Raksasa papiler conjunctivitis" dan "konjungtivitis Toxic" . (Lihat "Vernal keratoconjunctivitis" . meskipun seri berikutnya mencatat tingkat yang lebih rendah dari AKC pada pasien dengan AD.) EPIDEMIOLOGI AKC adalah penyakit mata alergi kronis yang paling sering terjadi pada pasien dengan riwayat dermatitis atopik [ 1. Konjungtivitis Toxic tidak alergi di alam. 4.org/publications/eyenet/201002/pearls. dimana VKC adalah "musiman" bentuk (setidaknya pada awalnya) dari AC yang dapat mempengaruhi kornea. tetapi sering bingung dengan penyakit mata alergi. karena tidak spesifik dan tidak dengan sendirinya membedakan AKC dari bentuk-bentuk lain dari penyakit mata atopik. VKC dibahas secara rinci secara terpisah. MD. bentuk yang paling umum dari alergi okular.2 ]. Prabjot Channa. http://www. di kisaran 20 sampai 40 persen [ 5 ]. (Lihat "alergi konjungtivitis: Manifestasi klinis dan diagnosis" . Ini mengembangkan dengan penggunaan berkepanjangan dari obat topikal. GPC dan konjungtivitis toksik dibahas secara rinci secara terpisah.

What Causes Itchy Eyes? Pruritus can be the chief complaint for a number of ocular surface diseases. Scott. It may be tempting to overlook this seemingly minor problem while assessing patients for potentially visionthreatening diseases. Conjunctival scrapings from patients with allergic conjunctivitis. review of systems and examination can help differentiate among these etiologies. and Sharon Fekrat. giant papillary conjunctivitis and contact dermatoblepharitis. which is why symptoms can take one to three days to manifest. contact lens–induced conjunctivitis. MD.  Allergic conjunctivitis and AKC are a result of IgE-mediated reactions that cause mast-cell degranulation and histamine release. as symptoms may result from a . A complete history. Although a physician’s inclination may be simply to treat the symptom with topical mast-cell stabilizers or antihistamines. it is important to identify the underlying cause.day quality of life. vernal keratoconjunctivitis. MPH. itchy eyes can be a major problem and source of anxiety for patients. the clinician can select an appropriate treatment regimen and provide patients with the relief they seek.  Blepharitis is also believed to have an immunologic basis. meibomian gland dysfunction. allergic conjunctivitis and atopic dermatitis are part of the spectrum of ocular allergies. MD (PDF 169 KB) Ocular pruritus is a common symptom that brings patients to the ophthalmologist’s office. Both type I (immediate) and type IV (delayed) hypersensitivity reactions are involved in vernal keratoconjunctivitis. often affecting their day-to. IgE-mediated processes as well as impaired cellular immunity and genetic factors also contribute to atopic dermatitis. Atopic keratoconjunctivitis.  Contact dermatoblepharitis is the result of a type IV T cell–mediated hypersensitivity reaction.Edited by Ingrid U. blepharitis. AKC and vernal keratoconjunctivitis will reveal eosinophils that are not part of the normal conjunctival histology. However. Other causes of pruritus include dry eye syndrome. By carefully and methodically determining the etiology of ocular pruritus. Pathophysiology Many of the causes of ocular pruritus are immunologically mediated.

 DES can be caused by either aqueous tear deficiency (either Sjögren or non-Sjögren type) or evaporative tear dysfunction (which includes MGD).reaction to staphylococcal antigens.  The etiology of conjunctivitis induced by contact lenses is multifactorial. these conditions are . Patients suffering from Sjögren syndrome also have autoimmune dysregulation.  Do your eyes burn and/or tear? Do you have foreign body sensation? All may be symptoms of dry eyes and/or MGD. including mechanical trauma.  Do you have asthma. The following questions may help narrow the differential:  Do your eyes itch throughout the year? Perennial complaints are often associated with allergic conjunctivitis and AKC. dry eye syndrome and hypersensitivity to contact lenses and/or solution as well as to protein deposits on the lenses. Acronyms AKC Atopic keratoconjunctivitis DES Dry eye syndrome GPC Giant papillary conjunctivitis MGD Meibomian gland dysfunction History A thorough history and review of systems should include special attention to onset. allergic rhinitis and/or eczema/skin rashes? A positive response may suggest allergic conjunctivitis. AKC and atopic dermatitis more strongly. duration and frequency of symptoms. as well as exacerbating factors and associated systemic complaints.  The pathogenesis of MGD involves the action of local inflammatory mediators in the setting of hyposecretion and obstruction of the meibomian gland orifices.

but the severity and location tend to vary.  Scaling of the eyelids. Patients with vernal keratoconjunctivitis tend to be more symptomatic in warmer climates. Examination A thorough examination will help reveal the underlying pathology. foamy tears. Eyelids.  Papillary reactions of the palpebral conjunctiva are seen with many of the aforementioned conditions. puckering and recurrent chalazia.frequently linked. soap or eyedrops? Itchiness caused by exposure to a sensitizing agent is often seen with contact dermatoblepharitis or blepharoconjunctivitis.  Blepharitis can result in crusting of the eyelid margin and collarettes at the base of the eyelashes. Soft contact lenses tend to induce more pruritus than rigid gas permeable lenses. such as creams. poorly fitting lenses and/or improper hygiene can lead to contact lens–induced conjunctivitis or GPC. Symptoms tend to develop within one to three days of exposure. eyelid margin telangiectasias. which can be seen with most of the conditions described.  MGD can cause inspissation of the meibomian gland orifices. makeup.  Have you used any new products. ectropion and leathery thickness of the eyelid (lichenification) are associated with atopic dermatitis and chronic contact dermatoblepharitis.  Can you identify any triggers? Exposure to pet dander or environmental allergens can often trigger allergic conjunctivitis.  Periorbital hyperpigmentation (“allergic shiners”) may point to an allergic cause.  Do you wear contact lenses? Contact lens overwear. Pay particular attention to the eyelids for:  Eyelid margin erythema and edema. .

 Varying degrees of mucoid discharge may also be seen. supportive treatment. while papillae are more prominent on the upper palpebral conjunctiva in contact lens–induced conjunctivitis. Small papillae tend to be located on both the upper and lower palpebral conjunctiva in AKC.  Marginal epithelial infiltrates can be present in MGD and contact lens–induced conjunctivitis. Pannus and corneal vascularization may be present and vary according to disease severity.  Horner-Trantas dots (raised. which are a common finding in the patient with itchy eyes. Contact reactions to topical carbonic anhydrase inhibitors and brimonidine are commonly delayed several weeks or months. Cornea. Exacerbations on the skin can be treated with corticosteroid cream or immunomodulators (e.g.” next page).. is usually sufficient. Ocular lubrication with artificial tears or ointment is also helpful. topical antihistamines and topical nonsteroidal anti-inflammatory drugs (e. Eliminate environmental and food allergens. Management and Treatment Once the diagnosis has been made. Patients with vernal keratoconjunctivitis may have giant papillae or diffuse papillary hypertrophy of the upper palpebral conjunctiva. Conjunctival signs include:  Mild to moderate bulbar conjunctival hyperemia and/or chemosis. Contact dermatoblepharitis/blepharoconjunctivitis. Additional therapies include the use of mast-cell stabilizers. it is imperative to identify and discontinue use of the offending agent. Topical corticosteroids applied to the eyelid can hasten recovery in more severe cases. tacrolimus) in severe cases. Conjunctiva.g. Once the irritant is eliminated. gelatinous collections at the limbus) and shield ulcers are classically associated with vernal keratoconjunctivitis. Moisturizing . which is seen in most cases of ocular pruritis. Atopic dermatitis. an appropriate treatment course can be selected (“Common Causes and Treatments for Ocular Pruritis. Check the cornea for:  Punctate epithelial erosions. ketorolac). including the use of cool compresses.. First.

. cromolyn sodium. However. Some patients may also require punctal plugs. olopatadine. therefore. Patients with AKC are more prone to infectious complications (especially herpes simplex keratitis) and should. oral and intranasal antihistamines and mast-cell stabilizers (e. refractive surgery is an alternative. Education regarding proper eyelid hygiene is imperative. naphazoline. Patients should first be advised to discontinue contact lens wear until the exacerbation has resolved. Consultation with an allergist for desensitization therapy may be necessary for those patients who remain symptomatic despite these measures. Vernal keratoconjunctivitis classically affects young men in warm climates. pheniramine. It is also appropriate to refit the lenses or to try different lenses and to advise patients about proper hygiene. mast-cell stabilizers are sometimes used as maintenance therapy. oxymetazoline) can be used on a short-term basis for symptomatic relief. Supratarsal corticosteroid injections have also been used to control symptoms. . Contact lens– induced conjunctivitis/ giant papillary conjunctivitis. Short-term use of a topical antibiotic (macrolides are often used) may be beneficial. Once again. Dry eye syndrome. Lubrication of the ocular surface is the ultimate goal. Topical vasoconstrictors (e. Once the exacerbation hasresolved. Topical corticosteroids and even immunomodulators (such as cyclosporine A) may be necessary. It may be helpful to change to daily-wear contact lenses. these patients tend to require more aggressive measures compared with those suffering from allergic conjunctivitis. topical (e.g.g. Shield ulcers may require plaque debridement and scraping at the ulcer base followed by aggressive treatment with topical corticosteroids and antibiotics. be monitored closely. it is important to avoid or eliminate allergic triggers whenever possible. Staphylococcal marginal keratitis will often require the use of topical corticosteroids to quell the inflammatory response. Initial treatment with artificial tears (if the tears are used more often than four times daily. Systemic antihistamines and mast-cell stabilizers may also provide relief. Symptoms may be alleviated with topical antihistamines and mast-cell stabilizers. Topical NSAIDs and corticosteroids should be used with caution and require frequent follow-up. For those who remain intolerant. these patients may find relief in cooler climates or air-conditioned environments. A clean washcloth dipped into baby shampoo diluted with water is commonly used for eyelid massage and scrubbing. then a preservative-free formulation is necessary) and with lubricant at bedtime. while some patients will require a course of oral tetracyclines that are then tapered off.g. lodoxamide) are often beneficial.. Ocular surface lubrication with artificial tears can provide additional relief. ketotifen). Allergic conjunctivitis. Warm compresses and twice-daily eyelid scrubs can help open inspissated meibomian glands. Artificial tears will help dilute any allergen remaining on the ocular surface.the facial skin (specifically the eyelid) is important for long-term treatment.. The use of physical barriers (such as glasses) is also useful in limiting allergen contact. is acceptable. Vernal keratoconjunctivitis/atopic keratoconjunctivitis. Meibomian gland dysfunction/blepharitis. Supportive care with cool compresses can be helpful for some patients. For patients with more severe symptoms. Those who remain symptomatic may need topical cyclosporine A to increase tear production.

cromolyn sodium.g. naphazoline. lodoxamide) Topical NSAIDS and corticosteroids Consultation with an allergist for desensitization therapy Vernal keratoconjunctivitis Topical antihistamines and mast-cell stabilizers Topical corticosteroids and immunomodulators (e.g... artificial tears Mast-cell stabilizers and topical antihistamines Topical NSAIDs (e.g..g. cyclosporine A) Supratarsal corticosteroid injection Atopic keratoconjunctivitis Similar treatment as for vernal keratoconjunctivitis Contact lens–induced conjunctivitis/giant papillary conjunctivitis Discontinue contact lens use Refit contact lenses Proper contact lens hygiene Refit contact lenses Mast-cell stabilizers for maintenance May consider refractive surgery in refractory cases Meibomian gland dysfunction/blepharitis Eyelid hygiene Artificial tears . tacrolimus) Lubrication of eyelids Systemic antihistamines and mast-cell stabilizers Dry eye syndrome Artificial tears and lubricating ointments Punctal plugs Topical immunomodulators (e. pheniramine.g. ketotifen) as well as oral or intranasal antihistamines. olopatadine.g.Common Causes and Treatments of Ocular Pruritus Contact dermatoblepharitis/ blepharoconjunctivitis Remove offending agent Cool compresses... oxymetazoline) for short-term symptomatic relief Topical (e.. and mast-cell stabilizers(e. cyclosporine A) Allergic conjunctivitis (seasonal and perennial) Remove offending agent Cool compresses Eyeglasses to shield from allergens Artificial tears Topical vasoconstrictors (e. ketorolac) and corticosteroids as needed Atopic dermatitis Remove offending agent Topical corticosteroid cream or immunomodulators for skin symptoms (e..g.

usually AKC.66 Three percent of the population has atopic dermatitis. Recent series of patients report the .67. in 1953.68 From 15% to 67..5% of patients with atopic dermatitis have ocular involvement. macrolides) Course of oral tetracyclines followed by taper Short course of topical corticosteroids https://www.g.inkling.com/read/cornea-krachmer-mannis-holland-3rd/chapter-49/atopickeratoconjunctivitis Atopic Keratoconjunctivitis Definition Atopic keratoconjunctivitis (AKC) is a bilateral.67–69 Demographics The onset of disease is usually in the second through fifth decade although the majority of patients with atopic dermatitis are diagnosed by age 5 years. Hogan.Topical antibiotics (e. chronic inflammation of the conjunctiva and lids associated with atopic dermatitis. was the first to describe the findings of chronic conjunctivitis and keratitis in patients with atopic dermatitis.

Subepithelial fibrosis is present in many.70.6 Tarsal margin keratinization 13 28.4 : 1 and less than 1. corneal.6 Meibomianitis 25 55.2 – – 16. of patients % 30 33 – – 6 – 18 – – 81.2 Blepharitis 25 55.73 Table49. conjunctival. This may be the principal manifestation in a minority of cases. in decreasing order of frequency. fornix foreshortening in some. and punctal ectropion. include watering.9 Symblepharon 12 26. gelatinous hyperplasia may occur (Fig. developing cicatricial ectropion and lagophthalmos. Lateral canthal ulceration.4 Conjunctiva Subepithelial fibrosis 26 57. Horner-Trantas dots have been reported to occur in AKC.3).72 Signs Signs of AKC include skin. redness. flaking dermatitis with a reddened base (Fig. In contrast to VKC.3 Punctal ectropion – – Ectropion 5 11. and pain.6 – – 26 – 10 11 70. and possibly a pale white edema (Fig. lid margin. and madarosis may also be present.2).7 . blurring of vision. The lids may become lichenified and woody.8 Fornix foreshortening 13 28. follicles. This may be more pronounced in certain seasons or it may be perennial. Other symptoms. and lens changes (Table 49.1 Entropion 2 4. The lid margins may show loss of cilia.0 29.72 Exacerbation of symptoms most frequently occurs in the presence of animals.9 Trichiasis 8 17.4 Tuft et al72 (N = 37) No.1 89. The conjunctiva of the tarsal surfaces has a papillary reaction.2 – 48. 49.2 Clinical signs in patients with AKC Foster and Calonge70 (N = 45) Condition No. A perilimbal.7 Giant papillae 11 24. 49. mucus discharge.5). meibomianitis. cracking.70–72 The male : female ratio is reported as 2. keratinization.8 Madarosis 6 13. the papillary hypertrophy of AKC is more prominent in the inferior conjunctival fornix.3 – 27. The periocular skin often shows a scaling. of patients % Lids Eczema 28 62.onset of symptoms between the ages of 7 and 76. The bulbar conjunctiva may have few findings besides erythema and chemosis. photophobia.72 No racial or geographic predilection is reported. 49.4). Symptoms Itching is the major symptom of AKC. and symblepharon in a few.

microbial ulceration.7–16.Condition Foster and Calonge70 (N = 45) No.80 This suggests an up-regulation of antigen presentation. 49. 100 64.80 Antibodies to HLA-DR stain diffusely throughout the epithelium.72 Anterior uveitis and iris abnormalities are not reported.7 Significant vision loss in this disease usually results from pathologic conditions of the cornea. Note the fornix foreshortening and pale edema. allowing pseudotubule structures to form. is an anterior or subcapsular cataract.4 1 Fig. since steroids are so frequently used in the treatment of the disease.2). 49.5 Limbal gelatinous hyperplasia in AKC.8 4 Filamentary keratitis 2 4. of patients % 6 13. Retinal detachment with or without previous cataract surgery is the principal posterior manifestation of AKC reported.4 Lower tarsal conjunctiva in AKC.82.8 2. however. Persistent epithelial defects.74 Herpetic keratitis is reported to occur in 14–17. Punctate epithelial keratopathy is the most common corneal finding. There is an increase in the CD4:CD8 ratio in AKC over normal conjunctival epithelium. scarring.70. Fig. and neovascularization are the main corneal causes for decreased vision (see Table 49.72 Keratoconus occurs in 6.83 . of patients % 5 13. In vivo confocal microscopy reveals fewer basal epithelial cells in the cornea.78 Mast cells in the epithelium of AKC patients contain predominantly tryptase as the neutral protease.9 10. Mast cells and eosinophils are found in the conjunctival epithelium of AKC patients but not in normal individuals. The lens opacity typically associated with AKC. Goblet cell density and squamous metaplasia are then examined by impression cytology.3 Tuft et al72 (N = 37) No. This cataract often has the configuration of a Maltese cross. The prevalence of cataract associated with AKC is difficult to determine.75–77 Pathophysiology Atopic keratoconjunctivitis is thought to consist of both type I and type IV hypersensitivity mechanisms.80 This increase of CD4 or helper T cells (Th) probably serves to amplify the immune response that is occurring.79 The epithelium may become involuted.2% of patients.3 37 Neovascularization 17 37. Penetrating keratoplasty typically results in similar surface problems but has been shown to improve vision in some. Evidence of the pathologic process comes from histologic and immunohistochemical analysis of conjunctival biopsy specimens and from tear fluid analysis for mediators and cells.70.5 Follicles Cornea Superficial punctate keratitis 24 53.81 Mucin proteins and mRNA are increased in the epithelium. Fig. 49.3 Severe periocular and lid involvement of AKC.8 24 Persistent epithelial defects 17 37.8% of patients.

B cells.95 Serum of AKC patients has been found to contain increased levels of IgE. AKC patients are usually older and have major lid involvement compared to patients with VKC. HLA-DR staining. There is usually a family history of atopic disease in one or both parents and commonly other atopic manifestations in the patient. Treatment The approach to treatment is multifaceted and includes environmental controls as well as topical and systemic medications.65. SAC patients have no or markedly diminished symptoms out of their season and show no evidence of chronic inflammation in the conjunctiva.87 Tears of AKC patients contain increased levels of IgE.69.85 A large number of mononuclear cells is present in the substantia propria. eosinophil neurotoxin. Fibroblast number is increased. History and examination reveal features to help differentiate AKC from other atopic ocular conditions. In addition. and there is an increased amount of collagen compared to normal individuals.83.96–98 Tabbara et al. never found in normal structures. The patient typically describes severe. eosinophil cationic protein. and IL-2 receptor. A Giemsa stain of a scraping of the upper tarsal conjunctiva may reveal eosinophils.87 Th2 cytokines predominate in allergic disease yet lymphocytes with Th1 cytokines have been found in the substantia propria of AKC patients. but the details of these cellular interactions remain speculative. The lack of contact lens wear aids in differentiating AKC from GPC. It is unlikely that the AKC patient will see the ophthalmologist . persistent. eosinophil neurotoxin. Furthermore. The significant past history or concurrent presence of eczema cannot be emphasized enough as a finding in patients with AKC. IL-4. are present in the substantia propria in AKC. specific sIgA. These eosinophils are found to have increased numbers of activation markers on their surface.The substantia propria in AKC has an increased number of mast cells compared to normal.70. eotaxin.80 The T-cell population of the substantia propria includes CD4 and memory cells. Conjunctival inflammatory cell density showed a negative correlation with tear stability and corneal sensitivity and a positive correlation with the vital staining scores.69.84 Eosinophils. activated B cells. IL-5. periocular itching associated with dermatitis.100 In summary. The serum level of IgE is often elevated in patients with AKC.88–94 AKC has reduced tear break-up time and decreased Schirmer’s values (56% less than 5 mm) compared to controls.71 A history of seasonal or exposure-related exacerbations is usually present. the substantia propria demonstrates increased CD4/CD8.27.99 Messmer and colleagues show eosinophils and their products deposited in the ulcers and stroma of corneas from AKC patients. Diagnosis Paramount to both diagnosis and treatment in AKC is a careful history.86. eosinophil cationic protein (reduced following papillae resection). and Langerhans cells. a complex immune cell profile implicates more than the mast cell alone. AKC patients demonstrate an increased number of conjunctival mast cells and evidence of mast cell activation. report adoptive transfer of AKC in bone marrow recipients. such as asthma (65%) or allergic rhinitis (65%).80 The T-cell receptor on lymphocytes in the substantia propria is predominantly of the α or β subtype. soluble IL-2 receptor. and osteopontin.

The topical administration of steroids such as prednisolone acetate eight times per day for 7 to 10 days is clearly beneficial in controlling symptoms and signs.55. The potent topical antihistamines offer much greater H1 receptor antagonism than over-the-counter antihistamines. Ciclosporin A and tacrolimus. nedocromil. There is potential for overuse due to the chronic nature of the disease. despite . These agents. The role of systemic desensitization is similar to that in VKC. if contributing in any way to corneal compromise.70 H1 receptors seem most responsible for the symptoms of AKC. and ketotifen may be helpful. or mast cell stabilizer combination antihistamines such as olopatadine. the patient must remove environmental irritants in both the home and the employment or school setting. Plasmapheresis has been shown effective in the treatment of AKC. tearing. must be corrected. However. Mast cell stabilizers alone such as cromolyn. Trichiasis or lid position abnormalities.109 Lid and ocular surface abnormalities may require treatment other than that directed toward the underlying pathologic condition of AKC. he or she must also be warned of the potential for causing cataract and glaucoma. its use should be initiated two to four times daily concurrent with a short burst of topical steroids (for 7–10 days). The patient must be instructed that steroid use must be transient only and must be carefully monitored for efficacy. of course. must be used judiciously. The nature of the irritants may be better defined through skin testing.104–108 Foster and Calonge recommend maximizing the use of systemic antihistamines. The topical application of a vasoconstrictor–antihistamine combination may bring transient relief of symptoms but is unlikely to intervene in the immunopathologic process or its sequelae. Only in rare cases of uncontrolled dermatitis with vision-threatening complications are oral steroids indicated.without also being under the care of a medical physician. Nonsteroid medications have been shown to be effective in reducing itching. lodoxamide. If an exacerbation occurs and the patient is not taking a mast cell stabilizing agent topically. azelastine. since the chronic nature of the disease may encourage overuse. both orally and topically. and photophobia. have been shown effective in treating AKC as well as reducing the amount of topical steroid use. Any staphylococcal blepharitis should receive adequate antibiotic treatment. If.101–103 Mast cell stabilizers two to four times daily is recommended year-round in patients with perennial symptoms. and newer antagonists are fairly specific for the H1 receptor. epinastine.