At a glance......
- 1 Types of Burning Eyes
- 2 Causes of Burning Eyes
- 3 Symptoms of Burning Eyes
- 4 Diagnosis of Burning Eyes
- 5 Treatment of Burning Eyes
- 6 Surgical Treatment
Burning Eyes Treatment/Burning eyes caused by a dry eye condition usually can be relieved with frequent use of lubricating eye drops (also called artificial tears). When selecting a brand of artificial tears, consider one that is preservative-free — particularly if you plan to use the drops frequently. If your discomfort continues, let your doctor know, since there are other dry eye treatments that may be more effective and also help relieve your burning eyes.
Types of Burning Eyes
|I||Corneal epithelial damage||No limbal ischemia||Good|
|II||Corneal haze, iris details visible||<1/3 limbal ischemia||Good|
|III||Total epithelial loss, stromal haze, and iris details obscured||1/3–1/2 limbal ischemia||Guarded|
|IV||Cornea opaque, iris and pupil obscured||>1/2 limbal ischemia||Poor|
Causes of Burning Eyes
- Blepharitis – Blepharitis is characterized by flaky, dandruff-like skin at the base of the eyelids. It is caused by a bacterial infection. Additional symptoms include eye redness and swelling.
- Dry eyes – Dry eyes can result when the tear ducts do not produce enough tears or the right kind of tears. Dry eyes tend to occur more often in women and older people. Additional symptoms can include – pain, eye redness, heavy-feeling eyelids, blurred vision
- Eye allergies – Also known as allergic conjunctivitis, eye allergies occur when irritating substances get into the eye. The body responds to these substances by producing histamines, which can cause burning eyes. Common triggers of eye allergies include dust, pollen, smoke, perfumes, pet dander, and foods. redness, tearing swelling, itching of the eyes
- Eye sunburn – Overexposure to the ultraviolet (UV) light from the sun’s rays can cause eye sunburn, which is also known as photokeratitis. In addition to burning eyes, symptoms include – light sensitivity, pain, a gritty feeling, watering, halos around lights
- Ocular rosacea – Ocular rosacea is a condition that causes inflammation of the eyelids. It affects people who have acne rosacea, a skin condition characterized by redness and flushing on the face. Additional symptoms of ocular rosacea include- pain, light sensitivity, vision loss in severe cases
- Pterygium – Pterygium is a growth of fleshy tissue on the white part of the eye. It usually occurs nearest to the nose, although it can also appear on the outer portion of the eye. It is thought to be caused by a combination of dry eyes and UV light, burning eyes, itching, redness, swelling
- In some cases – the growth can extend to cover the cornea, which can affect vision. If your burning eyes are accompanied by pain or excessive light sensitivity, or if you have any eye discharge, blurred vision, eye floaters or flashes of light, double vision or other unexpected symptoms, contact your eye doctor right away for immediate attention.
Symptoms of Burning Eyes
- Inflammation of Eyelid margin at the lash follicles
- Moderate lid swelling along the lash line
- Lower Eyelid is usually more affected
- Soft, oily Yellow Skin Scaling
- Local irritation and burning
- Watery eyes
- Red eyes
- A gritty, burning or stinging sensation in the eyes
- Eyelids that appear greasy
- Itchy eyelids
- Red, swollen eyelids
- Flaking of the skin around the eyes
- Crusted eyelashes upon awakening
- Eyelid sticking
- More frequent blinking
- Sensitivity to light
- Eyelashes that grow abnormally (misdirected eyelashes)
- Loss of eyelashes
Diagnosis of Burning Eyes
When a patient with bilateral and burning eyes is encountered, it is recommended that the following tests be routinely performed:
- Blood tests for vitamin B12 levels and serum cobalamin levels
- Levels of vitamin B12 metabolites (serum methylmalonic acid and plasma total homocysteine)
- Complete blood count (CBC) with smear analysis to rule out anemia, macrocytosis, and neutrophil hypersegmentation
- Levels of intrinsic factor and parietal cell antibodies to rule out pernicious anemia
- Red blood cell folate levels which are a more reliable indicator of tissue stores than serum folate level)
- Bilateral – painless subacute visual failure that develops during young adult life
- Visual acuity is severely reduced to counting fingers or worse in the majority of cases.
- Visual field testing by kinetic or static perimetry shows an enlarging dense central or centrocecal scotoma.
- Disk hyperemia – edema of the peripapillary retinal nerve fiber layer, retinal telangiectasia, and increased vascular tortuosityNote – Approximately 20% of affected individuals show no fundal abnormalities in the acute stage.
- Optic disc atrophy – Electrophysiologic studies (pattern electroretinogram and visual evoked potentials) demonstrating optic nerve dysfunction and the absence of retinal disease
- Postural tremor
- Peripheral neuropathy
- Movement disorders
- Multiple sclerosis-like illnesses
- Nonspecific myopathy
- Cardiac arrhythmias
Neuroimaging – Magnetic resonance imaging (MRI) is often normal, but may reveal white matter lesions and/or a high signal within the optic nerves.
- Pupillary reaction test – The doctor will shine a bright light in front of your eyes to see how they respond.
- Ophthalmoscopy – It checks your optic nerve to see if it’s swollen.
- Blood tests – They can find proteins in your blood that show you might be likely to get, or already have, neuromyelitis optic.
- Lumbar puncture – If both eyes are affected, if you’re under 15, or if your doctor thinks you have an infection, she might use this test to check the fluid that surrounds your brain and spinal cord. You might hear her call it a spinal tap.
- Optical coherence tomography (OCT) – It measures the fiber layer in your retinal nerve. If you have optic neuritis, it’ll be thinner than in people who don’t.
- Visual evoked response – The doctor attaches wires to your head with small patches. The wires record your brain’s responses as you watch a screen that displays an alternating checkerboard pattern. The test measures the speed at which your optic nerve sends signals to your brain. If it’s damaged, they’ll move more slowly.
Treatment of Burning Eyes
Treatments often aim at reducing eye dryness.
Other interventions a doctor may recommend for burning eyes include:
- Cleaning the eyelid margins near the base of the eyelashes, using a gentle cleanser and lukewarm water. A person can gently pat the eye dry following cleansing.
- Applying lubricating eye drops to reduce redness and improve eye comfort. For very dry eyes, a doctor may prescribe lubricating eye drops or artificial tears.
- Applying a warm compress to the eyes. Make a compress by soaking a clean, soft towel in warm water and then placing it over the eyes.
- Using antihistamine eye drops or tablets to reduce the effects of allergic reactions in the eyes. These products are available online.
- Taking supplements such as fish oil and flaxseed. These can help to reduce the effects of dry eyes. They are especially useful for people with ocular rosacea.
- Drinking plenty of water throughout the day can help to keep the eyes moist and reduce dryness.
- Taking regular breaks from using a computer screen can help reduce eye dryness and irritation.
- Wearing sunglasses to protect the eyes from UV light and further irritation.
Acute phase Treatment
Once the emergency treatment and evaluation are completed, the challenging task of healing the chemically injured eye begins. The major treatment goals that are important throughout the healing phases are:
- (a) reestablishment and maintenance of an intact and healthy corneal epithelium
- (b) control of the balance between collagen synthesis and collagenolysis and
- (c) minimizing the adverse sequelae that often follow a chemical injury. Acute phase treatment includes a broad-spectrum topical antibiotic, cycloplegic and antiglaucoma therapy. Apart from above-mentioned medications various therapies to promote reepithelization, support repair and control inflammation are used.
Modalities to Promote Reepithelization are
- Tear substitutes – Preservative free tear substitutes can ameliorate persistent epitheliopathy, reduce the risk of recurrent erosions and accelerate visual rehabilitation
- Bandage soft contact lens – Hydrophilic high oxygen permeability lenses should be preferred. They promote epithelial migration, helps in the basement membrane regeneration and enhances epithelial-stromal adhesion
- Retinoic acid – Has shown promise in the treatment of ocular surface disorders associated with goblet cell dysfunction
- Epidermal growth factor and fibronectin – Has a favorable effect on promoting epithelialization.
Drugs that Support Repair and Minimizing Ulceration
- Ascorbate – Ascorbate is an essential water-soluble vitamin that is a cofactor in the rate-limiting step of collagen formation. Supplementation of ascorbate by restoring depleted aqueous ascorbate levels reduces the incidence of corneal thinning and ulceration. Oral ascorbate (2 g/day) and topical 10% solution formulated in artificial tears are effective
- Collagenase inhibitors – Collagenase inhibitors promote wound healing by inhibiting collagenolytic activity and thus preventing stromal ulceration. Several collagenase inhibitors including cysteine, acetylcysteine, sodium ethylenediamine tetraacetic acid (EDTA), calcium EDTA, penicillamine and citrate have been reported to be efficacious. Only 10-20% acetylcysteine (mucomist) is available commercially. It is an unstable solution and has to be refrigerated and used within 1 week of its preparation.
Drugs to Control Inflammation
- Corticosteroids reduce inflammatory cell infiltration and stabilize neutrophilic cytoplasmic and lysosomal membranes. Use of topical steroids alone can potentially lead to a further increase in corneoscleral melt.[rx] Davis et al. evaluated patients with topical prednisolone 0.5% in conjunction with topical ascorbate 10% and concluded that there was not an associated increase in corneoscleral melt if topical steroids were used until reepithelization.[rx]
- The immediacy of treatment influences the final outcome favorably; hence, one should not delay the treatment waiting for careful assessment of the injury. After an acute chemical burn, immediate and extensive irrigation is necessary to wash out the offending chemicals [rx, rx, rx]. It is suggested to continue rinsing the eye for no less than 10 minutes [rx]. Irrigating contact lenses including Morgan Lens can also be used to provide ocular irrigation and/or medication to the cornea and conjunctiva after chemical burn [rx].
- Commonly, the ocular surface pH is checked using a urinary pH strip and irrigation is continued until pH normalizes to 7. Universal systems like amphoteric solutions (mostly Diphoterine) have less exothermic reactivity in addition to nonspecific binding capacity to bases and acids which makes them appropriate solutions for emergency neutralization [rx–rx].
- Any remaining particles are removed from the ocular surface with a moist cotton tip or fine-tipped forceps. Successful first line management of eye burns and adequate training of nonophthalmological emergency teams are imperative to ensure the best possible outcome. It is shown that prognosis is closely related to the efficiency of the immediate treatment measures [rx, rx].
- Preservative free tear substitutes and lubricating ointment can ameliorate persistent epitheliopathy, reduce the risk of recurrent erosions, and accelerate visual rehabilitation [rx]. Generally, burn patients benefit from systemic ascorbic acid which may promote collagen synthesis and wound healing [rx, rx, rx].
- Autologous serum tears which contain many factors that promote healing may be used to promote epithelialization [rx–rx]. Likewise, bandage contact lenses may be considered for delayed epithelial healing.
- Large-diameter gas-permeable scleral contact lenses, such as the prosthetic replacement of ocular surface ecosystem (PROSE) (originally called the Boston Scleral Lens), have been used after chemical or thermal injury in an inpatient setting [rx, rx–rx]. They can also protect the cornea from desiccation and friction of the eyelids via blinking .
- Topical corticosteroids play a critical role in controlling acute inflammation after chemical injuries. They reduce inflammatory cell infiltration and stabilize neutrophilic cytoplasmic and lysosomal membranes. They also help resolving anterior chamber as well as conjunctival inflammation [rx].
- The downside is that they also inhibit reepithelialization and collagen synthesis. The conventional belief is that topical steroids should not be used beyond 10 to 14 days, as they increase the risk of inhibition of collagenesis, worsening corneal thinning, and possible corneal perforation in alkali burns [rx, rx].
- However, this is primarily a concern in severe injuries with persistent epithelial defects; otherwise, corticosteroids can (and should) be used safely beyond 7–10 days if the epithelium has already closed [rx, rx].
- Citrate has been used successfully to prevent polymorphonuclear leukocyte migration into the burnt tissue, thus reducing the release of free radicals and proteolytic enzymes [rx, rx, rx]. Free radicals are formed by hydroxyl ions and may be scavenged by ascorbic acid and tocopherols [rx]. Cycloplegic drops can be considered to blunt the pain from iris-ciliary body spasm [rx].
Treatment of High Intraocular Pressure
- As mentioned, alkali injuries that reach the trabecular meshwork can lead to elevated intraocular pressure which can be easily overlooked [rx]. To minimize toxicity to the epithelium, oral aqueous suppression is generally preferred over topical agents.
- The ocular surface should be inspected daily for symblepharon formation. A symblepharon ring can be placed in the fornices to effectively prevent symblepharon formation [rx]. The largest size is preferable which provides good separation of the palpebral conjunctiva from the bulbar conjunctiva.
- Although the above measures can successfully prevent symblepharon formation in the acute phase, they cannot prevent the chronic cicatricial changes that lead to the formation of scarring and adhesions [rx].
- Corneal ulceration and melting tend to occur in the most severe injuries. Corneal thinning is potentiated by collagenases or matrix metelloproteinases, released from polymorphonuclear cells and other resident cells [rx].
- Proteinase inhibitors such as Aprotinin and collagenase inhibitors such as cysteine, acetylcysteine, sodium ethylenediamine tetra acetic acid (EDTA), calcium EDTA, penicillamine, citrate, and especially tetracyclines were found to prevent corneal thinning in chemically burned corneas [rx, rx, rx, rx–rx]. Systemic tetracycline may also boost healing of persistent corneal epithelial defects [rx, rx].
- The primary intention of early surgery in the face of a chemical ocular burn is to maintain the globe and promote reepithelialization. Surgical management starts with initial debridement of the necrotic material and continues with amniotic membrane transplantation and tectonic grafting if necessary.
- Late surgical interventions, on the other hand, are aimed at restoring the normal ocular surface anatomy and visual function. These include correcting eyelid abnormalities, management of glaucoma, limbal stem cell transplantation, and ultimately keratoplasty.
Amniotic Membrane Transplantation
- Amniotic membrane transplantation (AMT) can be used both as a graft which can provide a basement membrane for epithelialization and/or as a patch where it acts as a biological bandage contact lens [rx–rx]. It was shown that cryopreserved amniotic membrane transplantation to the entire ocular surface within two weeks of a chemical or thermal burn results in immediate pain relief and healing of epithelial defects in patients with grade II-III burns [rx]. In addition, it is often used as an adjunct to medical therapy to decrease ocular surface inflammation and reduce scarring [rx, rx, rx–rx].
- In severe, grade IV injuries, the loss of limbal vascularity may lead to anterior segment necrosis in addition to lack of reepithelialization and subsequent conjunctivalization of the cornea. Early intervention to reestablish the limbal blood supply may potentially prevent late complications [rx].
- Tenonplasty involves debridement of necrotic tissue and advancing viable, vascular Tenon’s layer to the limbus securing it to sclera, combined with AMT with or without lamellar corneal patch grafting. It has been shown to prevent further scleral ischemia and melting [rx, rx, rx].
Limbal Stem Cell Transplantation
- Limbal stem cells deficiency is one of the most visually significant long-term sequelae of severe chemical injuries. Patients suffering from chronic irritation persistent epithelial defects with clinical signs of corneal conjunctivalization may be considered for stem cell transplantation [rx, rx, rx, rx].
- In general, it is best to delay limbal stem cell transplantation (from the time of injury) as much as possible, since the more the ocular surface inflammation is controlled, the better the results would be. Likewise, it is advised to have all eyelid abnormalities (e.g., trichiasis and symblepharon) addressed before considering limbal stem cell transplantation [rx, rx, rx, rx].
- Limbal stem cells can be harvested from the patient (conjunctival-limbal autograft (CLAU) [rx] and cultivated limbal epithelial transplantation (CLET) [rx]), immediate family members including parents, siblings, or children (living-related conjunctival-limbal allograft (lr-CLAL)), or cadaveric eyes (keratolimbal allograft (KLAL)). Several surgical techniques have been described [rx, rx, rx–rx].
- CLAU is only possible in unilateral burns but invariably has excellent results, with complete regression of corneal neovascularization such that successful reepithelialization and functional vision are achieved in 80–90% of patients [rx, rx]. CLET is a very suitable surgical alternative in cases with total unilateral LSCD [rx]. In patients with bilateral ocular surface injury, lr-CLAL or KLAL are the available options. Harvesting tissue from one eye or both eyes of a first-degree relative provides fresh tissue with closer genetic composition
- Patient with total limbal stem cell deficiency after chemical burn who was successfully treated with conjunctival-limbal autograft (2 years after surgery).
- Tectonic penetrating keratoplasty (PKP) which is a surgical intervention of last resort in burn patients may be inevitable in cases with severe thinning, large descemetoceles, and impending or frank corneal perforation. Conventional lamellar keratoplasty (LKP) or deep anterior lamellar keratoplasty (DALK; Melles and Anwar techniques) can be performed for visual rehabilitation of patients with extensive stromal scarring [rx, rx].
- Most often, due to corneal scar formation and variability of corneal thickness and irregularity, conventional LKP and Melles techniques are preferred [rx]. Otherwise, full thickness transplants can be performed successfully, once the limbal stem cell deficiency has been addressed [rx].
- Artificial corneas undoubtedly can improve vision but should be considered in cases when PKP has failed or expected to fail (e.g., in the setting of extensive stromal vascularization) [rx–rx]. Currently, the Boston keratoprosthesis remains the main option in patients in which it has not been possible to restore corneal clarity and a normal ocular surface with any of previous measures [rx, rx].
- Their long-term risks, the need for life-long regular followups, and adherence to daily antibiotic prophylaxis are some of the issues that may make some patients less than ideal candidates for keratoprosthesis [rx, rx, rx]. The Boston keratoprosthesis study group found excellent anatomical retention in patients with a chemical burn [rx].
- Reported long-term complications include retroprosthetic membrane formation, intraocular pressure elevation and/or glaucoma progression, sterile corneal stromal necrosis or corneal thinning, infectious keratitis, persistent epithelial defect, retinal detachment, sterile uveitis/vitritis, and infectious endophthalmitis [rx–rx]. The osteo-odonto-keratoprosthesis (OOKP) surgery is one of the last resorts usually kept for patients with bilateral corneal blindness resulting from several ocular and systemic pathologies [rx].
- Indications include severe end-stage Stevens-Johnson syndrome, Lyell’s syndrome, epidermolysis bullosa, severe trachoma, chemical or physical injury, loss of lids, and multiple corneal graft failure. Other surgical alternatives available for treatment of such cases (e.g., ocular surface reconstruction with stem cell transplant) should be considered prior to OOKP surgery [rx].
Burning Eye Remedies
For fast relief consider these natural remedies at home:
- Rinse your eyelids with lukewarm water. Rinsing can remove allergens and irritants from your eye, reducing inflammation and dryness.
- Soak a cloth in warm water, and then apply the warm compress over closed eyes for a few minutes several times a day.
- Mix a small amount of baby shampoo with warm water. Dip a cotton swab into the water, and then use it to clean the base of your eyelashes. This method unclogs oil glands and minimizes inflammation.
- Drink more water to increase eye moisture and reduce dryness. Dry eyes can trigger stinging, burning, and irritation.
- Step away from the computer and give your eyes a break. Staring at a bright computer screen for hours may contribute to irritation and burning.
- Wear sunglasses to protect your eyes from the sun and wind.
- Eat more omega-3 fatty acids to alleviate dry eyes and burning. Good sources of omega-3 include salmon, tuna, anchovies, and sardines. You can also receive omega-3s from flaxseeds if you’re a vegan or vegetarian. Talk to a doctor to see if supplements are right for you.
- Run a humidifier to increase air moisture and relieve dry eyes.
- Apply cucumber slices over the affected eye to reduce inflammation, swelling, puffiness, and burning.