Peripheral Keratitis [TPA]

Peripheral Keratitis [TPA]

In many cases, a systematic review of the history and a deliberate plan of action with adequate follow up will likely ensure a satisfactory outcome for both the patient and the doctor.

Let’s take the case of Ms. PP, a 62 white female in moderate distress with moderate pain in both eyes of a constant nature and redness.  She had bilateral redness of both eyes with matted lashes and lids for the past month with no acute photophobia or extreme ocular pain. Coincidentally, she reports foggy vision. She denies trauma of either eye.

Her medical eye history is significant for two prior emergency department visits where topical antibiotic and non-steroidal inflammatory medications were prescribed. Both of these interventions did not resolve the condition.  She is s/p LAISK in each eye six months ago with 20/20 distant vision in each eye.

Her medical history includes: (1) Type 2 diabetes (chronic high blood levels of glucose) ; (2) Hepatitis C (an inflammation of the liver), (3) An eruption (skin “boil”) in her neck which was drained of a foul-smelling orange fluid by her daughter; (4) Posterior, neck, anterior chest, lower legs and left torso of an angry rash; (5) A nodular subcutaneous lesion on her forehead; and (6) persistent fatigue.

She is alert, aware,  cooperative and responsive and is appropriately dressed.  She reports no dysethesias or paresthesias  Socially, she lives her father who is her primary care giver. A parrot who never left the cage recently died and there are no other pets.  Her only trip outside of California was to the Hawaiian Islands about 3 months previously. She is a “social” cigarette smoker and is a non-drinker at this although only recently.

Medications consist of the following: (1) Glucophage; (2) Ciprofloxacin eye drdops;  (3)Acular eye drops.

The physical appearance shows a well-nourished female patient with protuberant midriff. Her vital signs were BP 91/72, Pulse 101, Respiration rate 16, Temperature 37.4° C, Weight 82.8 kg. Laboratories done just a few days prior to the eye visit are notable for ESR of 89 mm/hr ; Sodium 128 mEq/L; Elevated WBC count of 19.2.

The patient was an emergency department “work in”.  Here visual acuities were 20/200 in each eye with PHNI. Pupils were unequal but both were equally reactive. The EOMs were full.  Confrontation visual fields were normal in each eye.

The biomicroscopic examination show an intact corneal flap and opacification of the cornea from the 6:00 position right midway into the flap of the central cornea. The conjunctiva was congested with visible scleral vessels and injection generally in all four quadrants of the conjunctiva in either eye. Matting was evident in both upper and lower lashes and lids of both eyes. The upper lids were everted and there were no visible foreign bodies or significant hypertrophy.

Intraocular pressures were difficult but were noted to be below 18 by handheld Goldmann.  The fundus examination through normal pupils did not reveal a vitritis. Otherwise the rest of the fundus was difficult to visualize.

It was concluded that this patient had an advanced and aggressive form of peripheral sterile keratitis that appeared to be coincidental but not necessarily caused by diabetes, hepatitis or refractive surgery. The keratitis was most likely a result of staphylococcus bacteria from the lower lids that produces a toxin that inflamed the peripheral cornea inferiorly. She started on topical generic prednisolone acetate drops one drop in each eye, hourly while awake and continued the topical ciprofloxacin drops.

She was eventually followed up by infectious disease for the hepatitis C and was reported to have completely resolved in 30 days. The treating physician tapered the topical steroid after 2 weeks to four times daily each eye for 2 weeks, until she was completely off within 3 months.  

She presented seven months after my first visit with the following corneal appearance.

At this visit she is asymptomatic and is presently on Metformin, 1000mg, daily and interferon. Her best vision is OD +0.25 +1.25 Axis 080 20/25+ and OS +0.25 +0.50 axis 035 20/25+. The corneas were clear of any scarring and there were no epithelial breaks or staining.  The flaps were present and unremarkable. Dilated examination was negative for any diabetic retinopathy and the discs were not glaucomatous. IOPs were 15mm Hg in each eye which were slightly lower than pre-LASIK levels.

The occurrence of sterile infiltrates and peripheral keratitis is an uncommon occurrence in refractive surgery and if present, is a complication within a week of the procedure. ^1-7 Equally uncommon but not unheard of is peripheral corneal keratitis in association with autoimmune conditions such as sarcoidosis or rheumatoid arthritis. ⁸ In the case of hepatitis, a study of 50 hepatitis patients did not reveal a single case of peripheral corneal keratitis. ⁶ There are case reports to the contrary. The addition of significant Sjogren’s Syndrome may predispose an eye to peripheral keratitis.^9,10   Also possible is the use of  immunosuppressive anti-hepatitis therapy has previously noted retinal edema and retinopathy. ¹¹

In this case, the presence of a peripheral keratitis is baffling.  It is possible that the coincidental nexus of refractive surgery six months prior coupled with increased ocular surface abnormalities could be a stimulus for peripheral keratitis. ¹²  It is also possible that hepatitis (B or C) and immunosuppressive anti-hepatitis therapy with diabetes and chronic blepharitis could also add fuel to that an ideal setting for keratitis could be present..  Without a doubt, the delayed recognition of chronic blepharitis and its treatment aggravated the clinical picture.

In summary, the refractive surgical procedure may predispose an eye to ocular surface non-inflammatory (e.g. reduction in goblet cell density) abnormalities.  That alone, however is unlikely to create the clinical picture in this case.  It is possible that the immunosuppressive therapy of interferon, hepatitis and diabetes may also be contributory. In such complicated cases, the clinician should be watchful for any systemic or ophthalmic history that could be relevant. Further study could further elaborate this risk factor for peripheral keratitis.   

References:

1.            Al-Amry M. Severe bilateral paralimbal sterile infiltrates after photorefractive keratectomy. Middle East African Journal of Ophthalmology. 2014;21(1):83-85.

2.            Ambrósio RJMD, Periman LMMD, Netto MVMD, Wilson SEMD. Bilateral marginal sterile infiltrates and diffuse lamellar keratitis after laser in situ keratomileusis. Journal of Refractive Surgery. 2003;19(2):154-158.

3.            Bromley JG, Albright TD, Kharod-Dholakia B, Kim JY. Intraoperative and postoperative complications of laser in situ keratomileusis. Expert Review of Ophthalmology. 2012;7(1):25-31.

4.            Garg PMD, Chaurasia SMS, Vaddavalli PKMS, Muralidhar RM, Mittal VMDDNB, Gopinathan UP. Microbial Keratitis After LASIK. Journal of Refractive Surgery. 2010;26(3):209-216.

5.            Haw WWMD, Manche EEMD. Sterile Peripheral Keratitis Following Laser in situ Keratomileusis. Journal of Refractive Surgery. 1999;15(1):61-63.

6.            Jain AK, Sukhija J, Saini JS, Chawla Y, Dhiman RK. Hepatitis C virus-associated keratitis. Eye. 2004;18(2):131-134.

7.            Lahners WJMD, Hardten DRMD, Lindstrom RLMD. Peripheral keratitis following laser in situ keratomileusis. Journal of Refractive Surgery. 2003;19(6):671-675.

8.            Silva BL, Cardozo JB, Marback P, Machado FC, Galvão V, Santiago MB. Peripheral ulcerative keratitis: a serious complication of rheumatoid arthritis. Rheumatology International. 2010;30(9):1267-1268.

9.            Okuse C, Yotsuyanagi H, Koike K. Hepatitis C as a systemic disease: virus and host immunologic responses underlie hepatic and extrahepatic manifestations. Journal Of Gastroenterology. 2007;42(11):857-865.

10.          Meskin SW, Carlson EM. Mooren's-type ulceration associated with severe hidradenitis suppurativa: a case report and literature review. Ocular Immunology And Inflammation. 2011;19(5):340-342.

11.          d'Alteroche L, Majzoub S, Lecuyer A-I, Delplace M-P, Bacq Y. Ophthalmologic side effects during alpha-interferon therapy for viral hepatitis. Journal of Hepatology. 2006;44:56-61.

12.          Albietz JM, McLennan SG, Lenton LM. Ocular surface management of photorefractive keratectomy and laser in situ keratomileusis. Journal Of Refractive Surgery (Thorofare, N.J.: 1995). 2003;19(6):636-644.