Decision Making in Ophthalmology: An Algorithmic Approach Johan Zwaan
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Visual Loss77

Ekta Kakkar,
Kent L Anderson
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Abbreviations: PCR: Polymerase chain reaction; KOH: Potassium hydroxide
The cornea, as the most anterior part of the eye, is exposed to the atmosphere and prone to injury. A corneal ulcer results from an epithelial defect that exposes the stroma to the environment leading to degradation. Superficial epithelial defects are repaired by the migration and division of adjacent epithelial cells, while larger ulcers require inflammatory cells from vessels to produce granulation tissue for healing.
 
SYMPTOMS
  • Pain and foreign body sensation due to chemical effects of the toxins on exposed nerve endings
  • Lacrimation
  • Photophobia due to stimulation of the nerve endings
  • Blurred vision due to corneal haze
  • Redness due to congestion of corneal vessels
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Table 77.1   Common causes and treatment of infectious keratitis
Type of infectious keratitis
Most common pathogens
Common treatment
• Bacterial (46%)
 – Gram positive (83%)
Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pneumoniae
Topical vancomycin, cefazolin, and/or fourth-generation fluoroquinolone
 – Gram negative (17%)
Pseudomonas spp., Serratia spp., Proteus spp.
Topical tobramycin, ceftazidime, ceftriaxone, fourth-generation fluoroquinolone, and/or gentamicin
• Viral (28%)
Herpes (e.g. herpes simplex virus), varicella, adenovirus
Herpes simplex virus (HSV): Acyclovir, valacyclovir, and/or trifluridine
• Fungal (24%)
Fusarium spp., Aspergillus spp., Fumigatus spp., Candida spp.
Topical natamycin, amphotericin, and/or voriconazole
• Protozoan (2%)
Acanthamoeba spp., Microsporidium spp., Onchocerca spp.
Topical polyhexamethylene biguanide, chlorhexidine, diaminidines, aminoglycosides, and/or antifungal imidazoles/triazoles
Source: The corneal ulcer paper by Amescua et al.
 
SIGNS
  • Swollen eyelids
  • Marked blepharospasm
  • Conjunctival hyperemia and ciliary congestion
  • The ulcer starts as an epithelial defect with a grayish-white infiltrate that enlarges leading to stromal edema
  • Pupil may be small due to the associated toxin-induced iritis
  • Intraocular pressure may be elevated due to inflammation
 
CAUSES
Infection with bacteria, virus, fungus, or protozoa may cause a central corneal ulcer (Table 77.1). Noninfectious etiology include keratoconjunctivitis sicca, due to the lack of protective lysozyme and betalysin found in tears, decreased corneal sensation from neurotropic lesions, increased exposure in lagophthalmos or Bell palsy, chemical burns, and contact lens irritation.
 
DIAGNOSIS
For infectious keratitis, corneal scrapings are taken under topical anesthesia using a sterile instrument. Scrapings are taken from the edges and the base of the ulcer. The samples are microscopically examined using Gram and Giemsa stains, potassium hydroxide (KOH) preparation, and other specific media based on suspicion. Cultures should be grown for at least 7 days before declared negative, and susceptibility testing should be performed to guide therapy.
 
STAGES OF THE CORNEAL ULCER
  • Progressive infiltration: Polymorphonuclear cells and lymphocytes infiltrate the corneal epithelium and may eventually lead to necrosis of the involved tissue.
  • Active ulceration: Hyperemia of the corneal vessels leads to accumulation of purulent exudates. This also causes vascular congestion of the iris and ciliary body and iritis from absorption of toxins from the infection site. Exudate infiltration into the anterior chamber from the vessels of the iris and ciliary body may lead to hypopyon formation. Ulceration may progress further leading to corneal perforation.
  • Regression: Induced by the host immune response, both humoral and cell mediated, and treatment. Leukocytes neutralize and phagocytose any infecting organism and necrotic cells. Digestion of the necrotic tissue may initially cause an enlargement of the ulcer along with a superficial vascularization that stimulates the host immune response. Normal corneal epithelium will then begin to grow over the edges of the ulcer.
  • Healing: Corneal fibroblasts and endothelial cells of the new vessels lay granulation tissue underneath the epithelium. This causes thickening of the stroma and pushes the epithelium anteriorly. The degree of scarring may be variable. The ulcer is superficial, if it involves only the epithelial layer, but involvement 274of Bowman membrane leads to a resulting scar called a nebula. If the ulcer involves up to one-third of the corneal stroma or more, the scar is called a macula or leukoma.
 
TREATMENT
Corneal ulcers should be cultured and treated empirically with a topical antibiotic with both gram-positive and gram-negative coverages. Systemic antibiotics are usually not needed but may be used in fulminant cases. Other nonbacterial infectious ulcers should be treated with broad-coverage topical antimicrobials directed at the specific inciting organism. One percent atropine or cyclopentolate drops should also be started to control pain from ciliary spasm and prevent development of posterior synechiae. Vitamins and non-steroidal anti-inflammatory drugs (NSAIDs) may be used to promote healing and anti-inflammatory effects. If the ulcer progresses despite therapy, search for a noninfectious cause. Cauterization or a contact lens may prevent further progression. A corneal biopsy may be needed, if no cause is identified. Penetrating keratoplasty may be performed if the ulcer is refractory to treatment and continues to progress with imminent perforation.
 
COMPLICATIONS
Ulcer may lead to corneal perforation due to a pressure tear in Descemet membrane or sloughing of the entire corneal epithelium if the offending organism is highly virulent. Toxic iridocyclitis may develop, if the toxins are absorbed into the anterior chamber. Fibrous exudates that block the angle of the anterior chamber may lead to secondary inflammatory glaucoma. Corneal scarring may lead to permanent visual impairment ranging from blurring to total blindness.
 
FOLLOW-UP
Daily follow-up of patients is recommended until a response to medical treatment is noted. Once there is an improvement in symptoms, the ulcer characteristics, and the anterior chamber reaction, treatment and follow-up may be tapered.
BIBLIOGRAPHY
  1. Amescua G, Miller D, Alfonso EC. What is causing the corneal ulcer? Management strategies for unresponsive corneal ulceration. Eye. 2012;26:228–36.
  1. Bourcier T, Thomas F, Borderie V, et al. Bacterial keratitis: Predisposing factors, clinical and microbiological review of 300 cases. Br J Ophthalmol. 2003;87:834–8.
  1. Garg P, Rao GN. Corneal ulcer: Diagnosis and management. J Comm Eye Health. 1999;12:21–3.
  1. Khurana AK. Comprehensive Ophthalmology, 4th Edition. New Age International Ltd,  New Delhi: 2007.

  1. 275 Nijm LM. Seven clinical pearls for diagnosing and managing challenging corneal ulcers. Young Ophthalmologists (YO) Info. January 2010. Available at http://www.aao.org/yo/newsletter/201001/article04.cfm. [Accessed October 2013].