Central Sterile Corneal Ulceration Clinical Presentation

• In diagnosing this condition, differentiating between infectious and noninfectious etiologies is crucial. Since the clinical management of any corneal ulcer is dependent on its etiology, obtaining all of the salient factors (eg, endogenous, exogenous, local) is important. Therapies for sterile persistent ulcerations should be considered only after adequately addressing infectious and systemic factors.
• Key points to assess in obtaining the history of a patient with a corneal ulcer include the following:

  • Prior ocular history - Prior ocular and adnexal surgery, recurrent episodes or infections (eg, herpes), and corneal dystrophy
  • Past medical history - Immune status, collagen vascular diseases, systemic infections, diabetes, malnutrition, alcoholism, and chronic debilitating diseases
  • History of trauma - Foreign bodies and their origin (eg, soil, vegetation, water), chemical splashes, and lid lacerations
  • Contact lens use - Type, frequency, duration, overnight use, and hygiene
  • Medications - Ocular and otherwise
  • History of present illness - Duration, ocular symptoms (eg, degree of pain vs clinical impression), and chronicity
  • Social history - Patient from an area endemic for certain infectious processes, nutritional status, and any alcohol abuse
• The etiology of a sterile ulcer is often multifactorial; in this setting, identifying the coconspirators in this process is important. A thorough evaluation to identify potential factors, including medications (medicamentosa), impaired corneal sensation (neurotrophic), exposure (eg, lagophthalmos), and reduced tear production (sicca), is necessary in most cases of persistent noninfectious ulceration.

• The physical examination should begin with a gestalt impression of the entire patient, with attention to the following:

  • General health of the patient - Skin lesions, skeletal abnormalities, mental status, degree of discomfort, hearing aids, scars, and limitations to ambulation that may indicate a systemic illness
  • Local ocular adnexa and related organs - Eyelids, lacrimal system, blink rate, scars, mucous membranes (eg, lips/mouth, conjunctiva), orbit, symmetry, and evidence of inflammation or infection
  • Palpation - If indicated for orbital resiliency (thyroid/exposure), lymphadenopathy, and lacrimal or other adnexal masses
  • Observation - Lagophthalmos and blink rate
  • Assessment of vital signs of the eye - Visual function, corneal sensation, tonometry, pupil function, and motility of the eye (Corneal sensation should be checked prior to tonometry.)
• On slit lamp examination of the cornea, note the appearance of and evaluate the following:

  • Conjunctiva, sclera, and lids - Erythema, pattern of injection (ciliary flush, diffuse or deep), perilimbal nodules, discharge, lid closure, lid margin disease, and flipped upper lid to exclude foreign body and floppy eyelid syndrome
  • Tear film - Degree, symmetry, regularity, and presence of debris
  • Epithelium - Location of epithelial defect (localized or diffuse), regularity, and microcysts
  • Stroma - Thinning and presence/pattern of infiltrates (eg, ring, feathery, radial)
  • Endothelium - Keratic precipitates
  • Anterior chamber - Hypopyon and inflammation
  • Corneal sensation
  • Symmetry between the eyes
  • Fluorescein examination
  • Dilated examination (if necessary)

A thorough history and physical examination should allow a clinician to narrow down the differential diagnosis.

• Infectious causes (which need to be ruled out first) include the following:

  • Bacterial (focal infiltrate)
  • Fungal (vegetable matter, eg, branch; appearance of satellite lesions; feathery borders to infiltrate; chronic)
  • Acanthamoeba (contact lens wear, tap water, soil, severe pain out of proportion to the appearance, radial keratitis, ring ulcer)
  • Herpes simplex virus (history, dendrites, decreased sensation, disciform keratitis, increased intraocular pressure)
  • Herpes zoster virus (vesicles over dermatome; pseudodendrites, no true terminal bulbs; decreased sensation; increased intraocular pressure)
  • Contact lens related (infectious or noninfectious)
• Noninfectious causes include the following:

  • Chemical burns, including alkali/acid burn (check pH)
  • Thermal/radiation burns (history)
  • Sicca (filaments, Sjögren syndrome)
  • Neurotrophic (decreased sensation, may have minimal pain, rolled edges, oval, lower one half of cornea, may be quite thin, herpes zoster virus/herpes simplex virus, postsurgery, fifth-nerve palsy, chemical burns, abuse of topical anesthetics, neurotrophic keratitis, diabetes mellitus, multiple sclerosis)^[16]
  • Exposure (lagophthalmos, lid abnormalities, inadequate blink, facial palsy, proptosis, thyroid disease)
  • Medicamentosa (drops)
  • Atopic (history, follicles/papillae)
  • Vitamin A deficiency (primary deficiency due to prolonged dietary deprivation; secondary deficiency due to diseases that interfere with fat absorption and storage, eg, celiac disease, cystic fibrosis, cholestasis)
  • Basement membrane abnormalities (microcysts, evidence of map-dot-fingerprint or anterior stromal dystrophies, history of trauma, other dystrophy)
  • Factitious
• Immune-related causes (usually peripheral) include the following:

  • Wegener granulomatosis
  • Rheumatoid arthritis
  • Other collagen vascular diseases (indicated from history and associated systemic findings)