Ocular Symptoms and Signs - Painful or Burning Eye

RED, PAINFUL EYE

    Corneal Abrasions

               Corneal abrasions are usually the result of either trauma or an anatomic corneal defect that causes recurrent erosions. The overwhelming majority of patients will describe trauma with a foreign object immediately before the onset of symptoms. Patient with recurrent erosion from inadequate adhesion of the corneal epithelium to the basement membrane typically describe onset of tearing, pain and foreign body sensation upon awakening. A corneal epithelial defect that stains with fluorescein is the finding on slit lamp examination. Conjunctival injection and a swollen eyelid may also be present. It is important to evert the upper lid to ensure there is no retained subtarsal foreign body. Topical antibiotic should be given four times per day for one week. For non-contact lens wearers, erythromycin ointment or polymyxin B/trimethoprim is sufficient. Contact lens wearers need antipseudomonal coverage with ofloxacin or ciprofloxacin and should not use their lenses until the abrasion resolves. Patching is generally not recommended and is contraindicated in contact lens wearers. Rapidity of healing depends on the size of the abrasion, but generally most abrasions heal in two to three days.

Fluorescein staining helps demonstrate corneal abrasions even if a cobalt blue light source is not available.

    Corneal Ulcers

               Most corneal ulcers are caused by bacteria. Fungal ulcers should be suspected in cases of corneal injury with plant material. Acanthamoeba is seen almost exclusively in contact lens wearers and herpes viruses cause corneal ulcers with distinctive features on examination which will be discussed below. Pain, redness, photophobia, and foreign body sensation are the usual symptoms. The physician should ask about contact lens use, swimming with contact lenses, trauma, and a foreign body to the eye. A white or yellowish-white infiltration of the cornea with fluorescein staining of the overlying epithelial defect is the key finding. Herpes viruses often have a dendrite like appearance to their epithelial defects.

Corneal ulcer. In this case, the ulcer was sterile and was due to corneal anesthesia with subsequent breakdown of the epithelium, which could not heal. The eye was inflamed.

               An ophthalmologist should be consulted to obtain corneal cultures. If the patient is a contact lens wearer, their contact lens case and contact lens solution bottles should also be sent to the microbiology lab. The appropriate antibiotic therapy can range from polymyxin B/trimethoprim four times per day to fortified antibiotics every hour depending on the size and location of the bacterial ulcer. An ophthalmologist should make this determination. For fungal, Acanthamoeba and herpetic ulcer treatment, please see Table 3. Patients initially need daily follow-up to ensure the ulcer is improving and to rapidly implement the results of the cultures and sensitivities. If the ulcer is outside of the visual axis, recovery of vision is the norm. If the ulcer is in the visual axis, scarring may limit vision and corneal transplantation may be necessary for visual rehabilitation.

Table 3.  Treatment of Selected Ocular Diseases

Disease

Treatment

Fungal corneal ulcers

Natamycin 5% drops or Amphotericin B 0.15% drops initially every 1 -2 hours with a slow taper over weeks once infection is controlled.  Topical steroids should be avoided.  Consider adding oral fluconazole or voricanazole in severe cases.

Acanthamoeba corneal ulcers

Polyhexamethyl biguanide 0.02%, Chlorhexidine 0.02%, or Propamidine isethionate 0.1% drops every hour.  Discontinue contact lens wear.

Herpes Simplex epithelial keratitis

Trifluorothymidine 1% drops 9 times per day with tapering as lesions heal over 14 days; subsequent prophylaxis with oral acyclovir 400 mg BID

Herpes Zoster ophthalmicus

Intravenous acyclovir 30 mg/kg/day in 3 doses, for 7 – 10 days in severely immuncompromised individuals.  Famiciclovir 500mg PO TID or Valacyclovir 1g TID in immunocompetent patients or reliable, immunocompromised patients with less severe disease.  Bacitracin ointment to skin lesions.

Immune-recovery uveitis associated with healed CMV retinitis

Topical prednisolone acetate with frequency depending on severity. Periocular steroid injection for visually symptomatic cystoid macular edema or vitritis. Avoid intravitreal injection of triamcinolone acetonide.

Necrotizing herpetic retinitis

Intravenous acyclovir 1,500 mg/m2 of body surface area in three divided doses for 7 – 10 days (associated with high rate of failure); consider addition of foscarnet to improve efficacy.

Intravenous foscarnet and/or ganciclovir if no response to acyclovir, or patient judged to be severely immunocompromised; complete induction courses of both drugs, then place on maintenance therapy with oral valacyclovir or valganciclovir.

Adjunctive local therapy for severe disease: Intravitreal injections of ganciclovir 2.0 mg and/or foscarnet 1.2 to 2.4 mg three times per week for two weeks, then once or twice per week until lesions healed

Toxoplasmosis chorioretinitis

Oral pyrimethamine 200 mg load then 25 mg BID, sulfadiazine 2 g load then 1 g QID, clindamycin 300 mg QID, folinic acid 10 mg twice weekly or 5 mg daily, for 4 to 6 weeks.

Alternatives: 1) Oral trimethoprim-sulfamethoxazole DS plus clindamycin 300 mg QID for 4 to 6 weeks. 2) Oral atovaquone 750 mg TID, clarithromycin 500 mg BID for 4 to 6 weeks (sulfa-intolerant patients or those who are uncontrolled on clindamycin or clindamycin plus pyrimethamine).

Pneumocystis choroiditis

Intravenous trimethoprim (5 mg/kg)/ sulfamethaxazole (25 mg/kg) Q 8 hours for 3 weeks or intravenous pentamidine 4 mg/kg daily.

Syphilitic chorioretinitis

Intravenous aqueous penicillin G 24 million units per day for ten days.  Alternative: intramuscular procaine penicillin G 2.4 million units per day for ten days; must be given with oral probenecid 500 mg QID. Intravenous treatment preferred in HIV infection.

Tuberculous choroiditis

Oral isoniazid 300 mg daily, rifampin 300 mg BID, ethambutol 15 mg/kg daily, or other three or four drug regimen.

Bartonella retinitis

Oral doxycycline 100 mg BID and rifampin 300 mg BID for 4 - 6 weeks.

Bacterial endophthalmitis

Intravitreal injection of vancomycin 1 mg and ceftazidime 2.25 mg. Treatment of underlying infection if endogenous endophthalmitis.

Fungal endophthalmitis

Local: Intravitreal injection of amphotericin 5 micrograms or voriconazole 100 micrograms usually at the time of pars plana vitrectomy to clear vitreous fungal colonies.

Systemic: Oral fluconazole 200 to 400 mg daily or intravenous amphotericin in escalating doses. Alternative:  voriconazole 200 mg PO BID

Intraocular lymphoma

High-dose intravenous methotrexate with or without radiation therapy.

Intrathecal chemotherapy for CNS involvement.

Salvage therapy with intravitreal injection of methotrexate 400 micrograms weekly X 4, then monthly for one year, for sight-threatening disease.

    Anterior Uveitis

               More than half of the cases of anterior uveitis are idiopathic. Blunt trauma can cause a self-limited form of the disease. Being HLA-B27 positive is most common systemic association among adults while juvenile idiopathic arthritis is more prevalent in children. Sarcoidosis and other systemic inflammatory conditions can be causative even when the systemic signs of the illness have not yet appeared. Tuberculosis, syphilis, and herpes simplex are among the common infectious etiologies. Rifabutin and cidofovir are two drugs that can induce anterior uveitis.

This man had symptoms of iritis with pain and sensitivity to light. The irregular pupil and sectoral atrophy at the 4:00 o’clock meridian is typical for herpes simplex related recurrent iridocyclitis.

               Patients present with a painful red eye and photophobia. A review of systems to elicit history of associated systemic symptoms is crucial. Slit lamp examination needs to be performed to look for cell and flare in the anterior chamber. Keratic precipitates, white cell deposits on the corneal endothelium, are a suggestive finding. If the patient has a unilateral uveitis without any history of systemic symptoms, no work-up is needed. If the uveitis is bilateral or recurrent, a systemic work-up is indicated and should be directed by findings from the review of systems.

               Topical steroid is the usual treatment with the frequency of application dependent on the severity of disease. Cycloplegic drops such as scopolamine 0.25% or atropine 1% will help with photophobia. Periocular steroid injections are needed in cases refractory to drop therapy. Oral steroid therapy is rarely needed; it is reserved for cases that are unresponsive to periocular steroid therapy. Of course, infectious causes should be treated with drops and the appropriate systemic antimicrobials. Most initial episodes of unilateral anterior uveitis resolve within one or two weeks. If uveitis is recurrent, it may necessitate chronic immunomodulatory therapy and underlying systemic disease processes must be addressed.

    Scleritis

               About half of the cases of scleritis are idiopathic. Connective tissue diseases, particularly rheumatoid arthritis, Wegener’s granulomatosis , and relapsing polychondritis, are the most common systemic associations. Infections are a much less common cause: corneal ulcer pathogens can extend onto the sclera. Alternatively, some infections such as tuberculosis and Lyme disease can affect the sclera directly. Patients with scleritis describe severe, boring eye pain which often radiates to the forehead and head. This pain may keep them awake at night. Examination with natural light can reveal a bluish hue to the sclera along with dilation of blood vessels and redness. These dilated vessels do not blanch with 2.5% phenylephrine and do not move when the conjunctiva is moved with a cotton swab.

Diffuse anterior scleritis in a patient with Wegener granulomatosis. The eye was painful.

               Testing for the systemic disorders, directed by findings on history and exam, should be done in all cases of scleritis. Oral NSAIDs may be sufficient in milder cases, but oral steroids are often needed in moderate to severe cases. Recurrent scleritis may need systemic immunomodulatory therapy. Infectious causes are treated with systemic antibiotics. Scleritis can be a chronic disease requiring long term therapy. Patients need to be monitored for scleral thinning in areas of previous inflammation.

Figure.

    Acute Angle-Closure Glaucomamamamama

               Patients with acute angle-closure glaucoma have a sudden onset of pain, blurred vision and halos around lights. They often have associated nausea, vomiting and headache. Increased intraocular pressure, a closed angle with a shallow anterior chamber, and corneal edema are the usual findings. These patients should be referred to an ophthalmologist for gonioscopy to confirm diagnosis. Treatment consists of intraocular pressure control with drops and laser peripheral iridectomy.

BURNING

    Pterygia

               Pterygia are caused by elastotic degeneration of the conjunctiva from exposure to sunlight and dry, windy conditions. They are most commonly located on the inner corner of the eye. When they become inflamed, they cause burning, irritation and redness. On examination, an inflamed pterygium is a red, wing-shaped fibrovascular tissue that extends onto the cornea. Aggressive lubrication with artificial tears can often relieve symptoms. Pterygia that are in the visual axis and impairing vision can be removed surgically. Inflammation can recur, and patients are advised to avoid dry, windy conditions that can exacerbate this.

               Please see the sections on conjunctivitis, dry eyes and blepharitis.