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Ocular chemical burns
OVERVIEW: Chemical exposure to the eye can result in rapid, devastating, and permanent damage and is one of the true emergencies in ophthalmology
• Separate alkaline from acid chemical exposure:
• Alkaline burns - more severe, alkali penetrates and saponifies tissues easily, may produce injury to lids, conjunctiva, cornea, sclera, iris, lens, and retina
• Acid burns - usually acid does not damage internal structures since protein coagulation limits acid penetration. Injury often limited to lids, conjunctiva, and cornea.
System(s) affected: Nervous, Skin/Exocrine
Genetics: N/A
Incidence/Prevalence in USA: Estimated 300/100,000/year
Predominant age: 18-65
Predominant sex: Male > Female
SIGNS AND SYMPTOMS: • Mild burns:
• Pain and blurred vision
• Eyelid skin erythema and edema
• Corneal epithelial defects or superficial punctate keratitis
• Conjunctival chemosis, hyperemia, and hemorrhages without perilimbal ischemia
• Mild anterior chamber reaction
• Moderate to severe burns:
• Severe pain and markedly reduced vision
• Second and third degree burns of eyelid skin
• Corneal edema and opacification
• Corneal epithelial defects
• Marked conjunctival chemosis and perilimbal blanching
• Moderate anterior chamber reaction
• Increased intraocular pressure
• Local necrotic retinopathy
• In alkaline burns, can have initial pain which later diminishes
CAUSES: • Alkali:
• Ammonia (NH3)
• Lye (NaOH)
• Magnesium hydroxide [Mg(OH)2]
• Potassium hydroxide (KOH)
• Lime [Ca(OH)2]
• Acids:
• Hydrochloric (HCl)
• Hydrofluoric (HF)
• Acetic (CH3COOH)
• Nitrous (HNO2)
• Sulfuric (H2SO4)
RISK FACTORS: • Construction work (plaster, cement, whitewash)
• Use of cleaning agents (drain cleaners, ammonia)
• Automobile battery explosions (sulfuric acid)
• Industrial work (many possible agents)
• Alcoholism
DIAGNOSIS DIFFERENTIAL DIAGNOSIS: • Thermal burns
• Ocular cicatricial pemphigoid
• Other causes of corneal opacification
• Ultraviolet radiation keratitis
LABORATORY: None
Drugs that may alter lab results: N/A
Disorders that may alter lab results: None
PATHOLOGICAL FINDINGS: • Precipitation of glycosaminoglycans causes corneal opacification
• Saponification of cell membranes causes cell death
• Cation binding to collagen results in hydration, thickening, and shortening of collagen fibrils. This can mechanically elevate intraocular pressure.
SPECIAL TESTS: Measure pH of tear film with litmus paper or electronic probe (irrigating fluid with non-neutral pH [e.g., normal saline has pH of 4.5] may alter results)
IMAGING: Not necessary unless suspicion of intraocular or orbital foreign body is present
DIAGNOSTIC PROCEDURES: • Careful slit lamp examination, fundus ophthalmoscopy, tonometry, and measurement of visual acuity
• Full extent of damage from alkaline burns may not be apparent until 48-72 hours after exposure
TREATMENT APPROPRIATE HEALTH CARE: Emergency room with inpatient admission and ophthalmology consultation, depending on severity
GENERAL MEASURES: Copious irrigation and removal of corneal or conjunctival foreign bodies are always the initial treatment. Continue irrigation until the tear film is of neutral pH and pH is stable. Sweep the conjunctival fornices every 12-24 hours to prevent adhesions.
SURGICAL MEASURES: • Punctal occlusion for tear film preservation and corneal epitheliopathy
• Tarsorrhaphy for persistent epithelial defects
• Tissue adhesive (e.g., isobutyl cyanoacrylate) for impending or actual corneal perforation
• Conjunctival or limbal autograft transplantation for epithelial stem cell restoration
• Lamellar or penetrating keratoplasty for tectonic stabilization or visual rehabilitation
ACTIVITY: Ambulatory
DIET: Usual for patient
PATIENT EDUCATION: • Safety glasses
• Need for immediate ocular irrigation with any available water following chemical exposure to the eyes
MEDICATIONS DRUG(S) OF CHOICE: • Immediate treatment (any non-toxic irrigant):
• In hospital setting, sterile water, normal saline, lactated Ringer's solution are effective
• In the field, use what is available (tap water). Rapidity of irrigation is critical.
• Irrigation is continued until pH of superior/inferior cul-de-sac is neutral
• It is impossible to over-irrigate
• Further treatment: (depending on severity and associated conditions)
• Topical prophylactic antibiotics: Any broad spectrum agent, e.g., bacitracin-polymyxin B (Polysporin) ointment q2-4h, ciprofloxacin (Ciloxan) drops q 2-4h, chloramphenicol (Chloroptic) ointment q2-4h
• Tear substitutes: hydroxypropyl methylcellulose (Hypotears PF, Refresh Plus) drops q4h, carboxymethylcellulose (Refresh P.M.) ointment qhs
• Cycloplegics for photophobia and/or uveitis: Cyclopentolate 1% tid, or scopolamine 1/4% bid
• Anti-glaucoma for elevated intraocular pressure (IOP): latanoprost (Xalatan) 0.005% q24h or timolol (Timoptic) 0.5% bid or levobunolol (Betagan) 0.5% bid and/or acetazolamide (Diamox) 125-250 mg po q6h or methazolamide (Neptazane) 25-50 mg po bid and/or mannitol 20% 1-2 g/kg IV prn
• Corticosteroids for intraocular inflammation: Prednisolone (Pred-Forte) 1% or equivalent q1-4h for 10-14 days; if severe, prednisone 20-60 mg po qd for 5-7 days. Taper rapidly if epithelium intact by this time.
• Consider vitamin C (ascorbic acid) 500 mg po qid and/or acetylcysteine (Mucomyst) 10-20% top q4 h if corneal melting occurs
Contraindications: None
Precautions:
• For timolol and levobunolol - history of congestive heart failure or chronic obstructive pulmonary disease
• For acetazolamide and methazolamide - history of nephrolithiasis or metabolic acidosis
• For mannitol - history of congestive heart failure or renal failure
• For scopolamine - history of urinary retention
• Topical corticosteroids must be used with caution in the presence of damaged corneal epithelium as iatrogenic infection can occur. Daily follow-up or consultation with an ophthalmologist is recommended.
Significant possible interactions: Refer to manufacturer's literature
ALTERNATIVE DRUGS: Where available - topical fibronectin, epidermal growth factor, prokinase inhibitors
FOLLOW UP PATIENT MONITORING: • Depending on severity of ocular injury, from daily to weekly visits initially
• May be inpatient
• If on mannitol or prednisone, consider frequent serum electrolytes
PREVENTION/AVOIDANCE: Safety glasses to safeguard uninvolved eye
POSSIBLE COMPLICATIONS: • Persistent epitheliopathy
• Fibrovascular pannus
• Corneal ulcer/perforation
• Progressive symblepharon and entropion
• Neurotrophic keratitis
• Glaucoma
• Cataract
• Hypotony
• Phthisis bulbi
EXPECTED COURSE AND PROGNOSIS: • Depends on severity of initial injury
• Increasing amounts of limbal ischemia and corneal opacification correlate with poorer prognosis
• For severely injured eyes, permanent loss of vision is not uncommon
• Autologous cultivated corneal epithelium has been used for long term restoration of vision.
• Autologous nasal mucosal transplantation has also been successfully employed
MISCELLANEOUS ASSOCIATED CONDITIONS: Facial cutaneous chemical or thermal burns
AGE-RELATED FACTORS:
Pediatric: N/A
Geriatric:
• Compromised ocular surface from keratitis sicca or other disease associated with poorer prognosis
• Compromised corneal endothelium or pre-existing glaucoma may also complicate clinical management
Others: N/A
PREGNANCY: N/A
SYNONYMS: Chemical ocular injuries
ICD-9-CM: 940.2 Alkali burn of cornea and conjunctival sac
940.3 Acid burn of cornea and conjunctival sac
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