Ophthalmologic Manifestations of Herpes Simplex Clinical Presentation

  • Author: Robert H Graham, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Feb 14, 2012
 

History

  • Patients may present with the following:
    • Red eye
    • Pain
    • Photophobia
    • Tearing
    • Decreased vision
    • Skin rash (eg, eyelid)
  • History of previous episodes of herpes infection
  • History of corneal abrasion; contact lens wear; or previous nasal, oral, or genital sores
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Physical

Primary herpes infection of the eye typically is a unilateral blepharoconjunctivitis, characterized by vesicles on the skin of the lids, follicular conjunctivitis, preauricular adenopathy, and, sometimes, punctate keratitis.[3] After primary infection, recurrent disease may involve any or all layers of the cornea. Since both infectious responses and immune responses are responsible for ocular disease, it is better to classify the keratitis based upon both the anatomical location (ie, epithelial, stromal, endothelial) and the pathophysiology (ie, infectious, immune, neurotrophic). Based on this mechanism of classification, 4 major categories of herpes simplex keratitis exist.[4]

  • Infectious epithelial keratitis
    • Corneal vesicles: These are minute, raised, clear vesicles in the corneal epithelium that correspond to the vesicles on the skin surface. Within a few hours, these vesicles coalesce and erupt to form a dendritic or geographic ulcer. In immunocompromised individuals, they may coalesce without eruption, forming a raised dendrite without ulceration that shows reverse staining with fluorescein.
    • Dendritic ulcer: This is the most common presentation. The lesion reveals a linear branching pattern with terminal bulbs and heaped borders that contain live virus.
    • Geographic ulcer: As the dendritic ulcer widens, it loses its linear pattern and assumes a geographic form, with scalloped edges and heaped borders. This tends to occur in patients immunocompromised by the use of topical steroids or by diseases (eg, HIV).
    • Marginal ulcer: When a dendrite develops close to the limbus, its anterior stroma gets infiltrated by leukocytes from the limbal blood vessels, resulting in a dendritic lesion overlying an anterior stromal infiltrate. This often can be mistaken for a marginal staphylococcal ulcer.
  • Neurotrophic keratopathy: This is neither infectious nor immune in nature, but the result of abnormal corneal innervation and poor tear production. A nonhealing, oval epithelial defect develops. This defect has smooth borders, in contrast to geographic ulcers, which have scalloped borders. Over time, stromal ulceration and opacification develop under the epithelial defect. Corneal perforation can occur.
  • Stromal keratitis develops in 25% of patients with epithelial disease.[5]
    • Necrotizing stromal keratitis presents as necrosis and dense infiltration of the stroma, with an overlying epithelial defect. This is a result of direct stromal invasion by the virus. This entity may resemble bacterial or fungal keratitis. The use of topical corticosteroids without antiviral coverage is a risk factor in developing necrotizing keratitis.
    • Nonnecrotizing stromal keratitis also is called immune stromal keratitis and interstitial keratitis. An antigen antibody inflammatory response is believed to be triggered by retained viral antigens in the corneal stroma. Stromal infiltration with or without neovascularization occurs. The overlying epithelium is intact, unless a concomitant infectious or neurotrophic keratitis is present.
  • Endotheliitis is an immune reaction at the level of the endothelium that may occur months to years after an episode of infectious keratitis. Characteristic findings include keratic precipitates (KP), overlying stromal and possibly epithelial edema, and iritis. Unlike stromal edema from primary stromal keratitis, no stromal infiltrates or neovascularization is present. Patients present with pain, photophobia, and injection. Based on the distribution of the KP, 3 recognized forms of endotheliitis can be identified.
    • Disciform endotheliitis presents as a round area of central or paracentral stromal edema overlying an area of KP.
    • Diffuse endotheliitis presents with scattered KP and diffuse edema.
    • Linear endotheliitis: Keratic precipitates develop in the peripheral cornea and proceed centrally. Associated corneal edema is isolated to the peripheral corneal stroma and epithelium.
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Causes

Primary herpes keratitis is a ubiquitous disease with no apparent risk factors. Recurrent infection due to reactivation and, occasionally, reinfection can be triggered by many events, including the following:

  • Stress
  • Sunlight
  • Fever
  • Menstruation
  • Trauma, including surgical trauma (eg, lamellar keratoplasty, peripheral iridectomy)[6, 7]
  • Antiglaucoma medications (ie, latanoprost, travoprost, bimatoprost[8] ); because of their ability to induce the release of endogenous prostaglandins in the iris and the ciliary muscles, prostaglandin analogues may induce reactivation of HSV keratitis.
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Contributor Information and Disclosures
Author

Robert H Graham, MD  Senior Associate Consultant, Department of Ophthalmology, Mayo Clinic, Scottsdale, Arizona

Robert H Graham, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, and Arizona Ophthalmological Society

Disclosure: WebMD/eMedicine Salary Employment

Coauthor(s)

Kerry Assil, MD  Medical Director and CEO, The Sinskey Eye Institute

Kerry Assil, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, Association for Research in Vision and Ophthalmology, and Contact Lens Association of Ophthalmologists

Disclosure: Nothing to disclose.

Specialty Editor Board

Kilbourn Gordon III, MD, FACEP  Urgent Care Physician

Kilbourn Gordon III, MD, FACEP is a member of the following medical societies: American Academy of Ophthalmology and Wilderness Medical Society

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD  Associate Professor of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Christopher J Rapuano, MD  Professor, Department of Ophthalmology, Jefferson Medical College of Thomas Jefferson University; Director of the Cornea Service, Co-Director of Refractive Surgery Department, Wills Eye Institute

Christopher J Rapuano, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, Cornea Society, Eye Bank Association of America, International Society of Refractive Surgery, and Pan-American Association of Ophthalmology

Disclosure: Allergan Honoraria Speaking and teaching; Allergan Consulting fee Consulting; Alcon Honoraria Speaking and teaching; RPS Ownership interest Other; EyeGate Pharma Consulting fee Consulting; Bausch & Lomb Honoraria Speaking and teaching; Bausch & Lomb Consulting; Merck Honoraria Speaking and teaching

Lance L Brown, OD, MD  Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD  Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Anisha Judge, MD, to the development and writing of this article.

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