Patients Name Initials: KKH                       AGE: 28         Date Patient Seen: 05/05/2014

Symptoms and History

A 41 year old African American male presented to the hospital eye clinic on May 5, 2014 with the complaint of a foreign body sensation in the left eye when blinking. The patient denied ocular hyperemia, or any changes in visual acuity, discharges or pain, or any lacrimation. The patient remembered similar symptoms in the not so distant past affecting both his right and left eye. He further added that his most recent ocular examination was conducted 3 months earlier although he admitted to non-compliance with the recommended medical follow-up.

The patients’ ocular historyincludedpresbyopia as well as suspicion of glaucoma.He refuted past ocular trauma or surgery. The ocular history of his family reflected evidence for glaucoma (mother). The medical history of the patient was positive for neurotic depression, and coronary artery disease as well as cervical radiculopathy. The patient could not remember his systemic medications. His social history was negative for recreational drug abuse, alcohol or tobacco. In addition, he had no known allergies for food or drugs. The patient was oriented to place, time, and person, and his mood were appropriate.

Clinical Findings

Uncorrected distance visual acuity was 20/20 OS and 20/20 OD. Habitual spectacle correction as measured by lensometer indicated Plano sphere OS, Plano sphere OD, with an add of +2.50 OU. Measured by manifest spectacle, correction reflected the same powers. Near visual acuity with correction was 20/20 OS and 20/20OD. The patient’s pupils were round and reactive to light, and equal.The examination noted no afferent pupillary defect. In both eyes, confrontation fields were full to finger counting. Extraocular muscles showed no restriction in all gazes without diplopia or pain. The cover test at near and distant was orthophoric. The patient showed no evidence of preauricular lymphadenopathy.

A cotton wisp test was negative for decreased corneal sensitivity. Goldman Applanation tonometry measured 12mmHg OS, OD at 10:56am. Slit lamp biomicroscopy disclosed normal adnexae, puncta, lashes, and lids as well as bulbar and palpebral conjunctivae in both eyes.The right corneal seemed normal, although the left eye exhibited numerouswhitish, surface, stellate, intersperse, epithelial cornealacerations.Staining of sodium fluorescein was positive in the left eye. The anterior chambers of both eyes seemed quite with no indication of flare or cell: assessment of the chamber angles reflected 4/4 using the Von Herrick method.  Both irides were brown and flat. Using a drop of 2.5% phenylephrine and 1% mydriacyl thepatient’spupils were dilated. An assessment of the posterior segment showed 1+ nuclear sclerosis of the lens in both the right and left eyes with the right eye showing peripheral cortical spoking.Fundus assessment displayed optic nerves with a cup-to-disc ratio of 0.70/0.65OS and 0.80/0.85OD.The cups were deep; there was no indication of edema of the neuroretinal rim or pallor. The right macula revealed traces of hard drusen; both maculae were flat. The vitreous was optically clear in both eyes. The vasculature was usual and the retinal periphery was flat with no breaks in both the right and left eye.

Differential Diagnoses

1. Herpes zoster viral (HZV) keratitis
2. Corneal ulcer
3. Thygeson superficial punctate keratitis (TSPK)
4. Epidemic keratoconjunctivitis (EKC)
5. Bacterial keratitis
6. Herpes simplex viral (HSV) keratitis
7. Acanthamoeba keratitis (AK)
8. Dry eye syndrome (DES)

HZV keratitis normally exhibits unilaterally with analogous symptoms as showed by HSV Keratitis, together with corneal pseudodendritis. Symptoms may also consist of skin lesion in the area along the branches of the cranial nerve V most often affecting the V1 and V2 dermatomes as well as facial pains.

Corneal ulcers usually exhibit hyperemia, pain, minimal to severe discharge, photophobia as well as reduced visual acuity subject to the location of the lesion.  Corneal lesions stain with the use of sodium fluorescein and may also demonstrate infiltration and edema with or with no anterior chamber retort.

TSPK embroils a slight to middling foreign body feeling, lacrimation that is minimal, as well as intermittent moments of photophobia.  Additionally, an asymmetrical presentation of many round and stellate regions of gray and slightly elevated intraepithelial corneal opacities can also be observed in either eyes or one eye.

EKC presents as an acute follicular conjunctivitis coupled with a waterysecretion, preauricular lymphadenopathy, hyperemia, and chemosiscoupled with non-staining subepithelial corneal infiltrates. Sometimes there can be an observation of pseudomembranes.

Bacterial keratitis normally is exhibited by photophobia, hyperemia and acute pain. In some cases there is a ropy, thick, and mucopurulent discharge, and a stromal infiltrate with an overlying epithelial excavation.

HSV keratitis normally is characterized by a unilateral “red eye” coupled with up-and-down levels of pain or ocular irritationwhich are usually linked with photophobia and lacrimation, as well as reduced sensitivity of the corneal.  Dendritis manifested as epithelial corneal lesions are usually present in a tree-branching pattern and usually stain with sodium fluorescein.

AK is a parasitic disease of the corneal that is exhibited with severe pain, photophobia, hyperemia, ulcerations or infiltrates, and in advace circumstances displays radial neurokeratitis.

DES is symptomized by an irritation, foreign body sensation, burning and lacrimation, in addition to vision that is blurred which changes or improves with blinking. Acute infections may exhibit positive staining corneal puntate epithelial erosions.

Diagnosis

The presence of the corneal lesions in the left eye alludes to a diagnosis of TSPK based on the following:

1. Numerous,surface, slightlyraised, stellate lacerations which stain with sodium fluorescein dye;
2. No involvement of the conjunctivas;
3. No reaction in the anterior chamber; and
4. A history of recurrence

Management plan

He was started offon a maintenance dose of Restasis® (Cyclosporine A) 1% ophthalmic emulsion, a single drop thrice per day in both eyes ; as well as Vexol® (Rimexolone) 1% ophthalmic suspension, one drop per day in the right eye and four times per day on the right eye.

The patient was booked for a follow-up in seven days. Additionally, a diagnosis of a glaucoma suspect secondary to a large cup-to-disc ratio and family history of the disease was made. Therefore, a cirrus OCT of the optic nerves and pachymetry and a Humphrey visual field 30-2 SITA standard test was directed to assess the risk of glaucoma. Previous eye records were also asked for.Further, presbyopia, non-visually significant cataracts in both eyes and macular drusen in the right eye were also evaluated. The findings would be observed during future visits.

Follow Up Number 1

After 7days, the patient returned for an evaluation of the anterior segment. His left eye had registered complete resolution of symptoms, and the patient reported compliance with the advised therapy. His visual acuity remained stable, and the lesions which had previously been noted in his left eye had completely resolved. To prevent any likelihood of recurrence, he was directed to continue with the Restasis and Vexol medication for a further 7 days, after which a follow-up examination would be conducted.

Follow Up Number 2

The patient revisited for a follow-up anterior segment evaluation. He complained of reactivation of symptoms and acknowledged non-compliance with the therapy medication. His visual acuity was normal, with a slit lamp biomicroscopy revealing normal lashes, anterior chambers, lids, conjunctivae, and irides in both the right and the left eye. However, an assessment of the left eye revealed five, stellate, round regions of peripheral, coalescent SPK.Taking this recurrence into account, the patient was directed to increase his medical dosage of Vexol to a drop after every 3 hours in the left eye. The dosage of Vexol in the right eye remained unchanged. The dosage of Restasis remained unchanged. It was emphasized to the patient that compliancetothe medication was critical.

Follow Up Number 3

After 7 days, the patient returned. He reported complete compliance with the medical dosage and his symptoms had completely resolved. Evaluation of the anterior segment revealednormal sight.Taking into consideration the history of reoccurrencein a short period of time, the patient was directed to maintain the same dosage for an additional 7 days, and compliance with the medication was emphasized.

Follow Up Number 4

After 7 days, the patient returned for an anterior segment evaluation.  The patient reported complete compliance and revealed no symptoms. His visual acuity was stable, reporting uncorrected distance visual acuities of 20/20 OS,OD, with a slit lamp biomicroscopy revealing normal lashes, anterior chambers, lids, conjunctivae, and irides in both the right and left eye. Through a Goldmann Applanation Tonometry, the patient’s intraocular pressure measured 12mmHg OS and 13mmHg OD.

He was directed to maintain the Vexol dosage at a drop per day in his right eye while decreasing the Vexol dosage his left eye to one drop 4 times daily. Restasis was maintained at three times daily in botheyes. A glaucoma work-up and anterior segment evaluation were scheduled in the following follow-up slated in 7 days.

The patient did not attend the follow-up visit since he moved his care out of state.

Discussion

The clinical conditionreferred to as Thygeson Superficial punctate keratitis was first conceived by P. Thygeson in 1950(Nagra, Rapuano, & Cohn, 2004). It was perceived as a transient, commonly bilateral illness, that presented course corneal epithelial opacities with no indication of stromal involvement or edema of the corneal. It still remains a diagnosis of unclear etiology.Superficial examination of the eyes seems normal with no indication of swelling or infection of the conjunctiva. However, biomicroscopyexamination reveals several stellate regions of white-gray, somewhat elevated intraepithelial opacities that stain brightly with sodium fluorescein. According to Watson, Hollingsworth, & Tullo(2003), the opacities are transitory and often transform in form over time. The lacerations may bear a resemblance to pseudodendrities or subepithelial infiltrates, and asensation in the Cornea is normal. Examination of the anterior chambers exhibits the absence of flare.

The age of onset of TSPK symptoms can be as early as at the age of 2 years and as old as the age of 71 years(Nagra, Rapuano, & Cohn, 2004). The duration of TSPK may last up to 41 years typified with remissions and exacerbations. As TSPK symptoms settle, a person’s visual acuity returns to normal with no visual sequallae.According to Watson, Hollingsworth, & Tullo(2003), there are five diagnostic criteria that differentiate TSPK from other forms of epithelial keratitis. These,the authors outlines as: an extended duration of remissions and exacerbations; a persistent and two-sided punctate epitheliopathy; no positive reaction to antibiotics; corneal epithelial healing without scars; and a response to corticosteroids.

Various approaches to treatment of TSPK have been propositioned. These range from non-preserved artificial tears, topical corticosteroids, topical antivirals, bland ophthalmic ointments, topical cyclosporine A, andsoft bandage contact lenses. Corneal surgery has also been proposed (Reinhard, Roggendorf, & Fengler, 2004). Treatment is only directed to persons who have considerableirritation or blurred vision. This is for the reason that therapeutic side effects may result, which includes cataracts and glaucoma.

Conclusion

This case demonstrates the difficulties in the diagnosis and care of TSPK.  The decision on corticosteroid therapy was founded on previous successes of the approach which resulted in quick and improved patient comfort. However, extended use of this therapy presents increased risk to other diseases such as cataracts or glaucoma. It therefore becomes imperative for patient education and compliance so that such complications can be prevented and chances of a reoccurrence of the diseaseare minimized.

References

Goldberg, B. D., Schanzlin, D. J., & Brown, S. I. (n.d.). Management of Thygeson’s Superficial Punctate Keratitis. American Journal of Ophthalmol, 22-24.

Goldstein, M. H., Feistmann, J. A., & Tariq, B. M. (2002). PRK-PTK as a Treatment for a Patient with Thygesons Superficial Punctate Keratopathy. CLAO, 425-426.

Nagra, P. K., Rapuano, M. D., & Cohn, E. J. (2004). Thygeson’s Superficial Punctate Keratitis: Ten Years Experience. Ophthalmol, 34-37.

Reinhard, T., Roggendorf, M., & Fengler, I. (2004). PCR for Varicella Zoster Virus Genome Negative In Corneal Epithelial Cells of Patients with Thygeson’s Superficial Punctate Keratitis. Eye, 304-305.

Thygeson’s Superficial Punctate Keratopathy. (n.d.). Retrieved from Handbook of Ocular Disease Management: http//:www.revoptom.com/handbook/sect3j.htm.

Watson, S. L., Hollingsworth, J., & Tullo, A. B. (2003). Confocal Microscopy of Thygeson’s Superficial Punctate Keratopathy. Cornea, 294-299.

 
Do you need an Original High Quality Academic Custom Essay?