2c:I[856015,["/_next/static/immutable/chunks/1xzisbplk9czp.js","/_next/static/immutable/chunks/3j2i1faptc_-9.js","/_next/static/immutable/chunks/1bqb83_yclja0.js","/_next/static/immutable/chunks/1on664om2hmh1.js","/_next/static/immutable/chunks/30t4sjq-27eg7.js","/_next/static/immutable/chunks/08tq8rmv423j5.js","/_next/static/immutable/chunks/32zk736rs0hqw.js","/_next/static/immutable/chunks/0lbgs964whs_0.js","/_next/static/immutable/chunks/1a_hqhrsle_n_.js","/_next/static/immutable/chunks/0hcnvyarhzl7i.js"],"default"] 2d:T5e05,

Summary Table

Category	Details
Risk Factors	Industrial workers (cleaning agents, cement, fertilizers), laboratory personnel, assault victims, household accidents (drain cleaners, bleach, ammonia), battery explosion (sulfuric acid)
Etiology	Direct ocular surface contact with an alkaline substance (most common and most severe) or acidic substance; alkali causes liquefactive necrosis with deep penetration, acid causes coagulative necrosis with self-limiting penetration
Patient Presentation	Acute onset of severe eye pain, tearing (epiphora), blepharospasm, blurred vision immediately following chemical exposure
Classic Physical Exam	Conjunctival injection and chemosis, corneal epithelial defects or opacification, limbal blanching/ischemia (white, avascular limbus = severe injury), perilimbal blanching in a "porcelain white" appearance in Grade IV injuries; paradoxically, the most severe burns may appear deceptively "quiet" because of total vascular destruction
Key Diagnostic Results	Litmus paper pH testing of the conjunctival fornix (normal = 7.0 to 7.3); slit lamp examination showing corneal clarity or haze, fluorescein uptake for epithelial defects, assessment of limbal ischemia in clock hours; elevated intraocular pressure (IOP)
Management	Immediate copious irrigation with any available isotonic fluid BEFORE any other intervention; continue until pH normalizes (7.0 to 7.3); subsequent treatment includes topical antibiotics, cycloplegics, topical ascorbic acid, topical steroids (with time-limited use), and surgical referral for Grade III to IV injuries
Keywords	"Splash of cleaning fluid," "cement in the eye," "white/blanched limbus," "copious irrigation," "check pH," "porcelain white eye," "limbal ischemia," "alkali is worse than acid"

1. Pathophysiology

Chemical ocular burns involve direct destruction of the ocular surface, and their severity depends entirely on the type of chemical (alkali vs. acid), concentration, duration of contact, and area of exposure.

Alkali burns are the most dangerous because alkali agents are lipophilic. They dissolve and saponify cell membrane lipids, allowing the chemical to rapidly penetrate through the corneal epithelium, stroma, and even into the anterior chamber. This process is termed liquefactive necrosis, where tissue is progressively dissolved rather than sealed off. The alkali ion continues to penetrate deeper as long as contact persists. Common alkali agents include ammonia ($NH_3$), sodium hydroxide (lye/NaOH), calcium hydroxide (lime/cement), and potassium hydroxide (KOH). Because of this deep penetration, alkali burns can damage the lens (causing cataract), ciliary body, and trabecular meshwork (causing secondary glaucoma).

Acid burns, in contrast, cause coagulative necrosis. The acid denatures and precipitates surface proteins, forming a coagulum barrier that impedes further penetration. This is why acid injuries tend to be self-limiting and less destructive to deeper structures. The exception is hydrofluoric acid (HF), which behaves like an alkali because the fluoride ion penetrates deeply into tissues.

The critical structure that determines prognosis is the limbus, the zone between the cornea and sclera that houses the limbal stem cells. These stem cells are responsible for corneal epithelial regeneration. When limbal stem cells are destroyed by chemical injury, the cornea cannot re-epithelialize, and conjunctival tissue grows over the corneal surface instead (a process called conjunctivalization or limbal stem cell deficiency). The degree of limbal ischemia, visible as a white, avascular ring around the cornea, is the single most important prognostic indicator.

Inflammatory mediators released from damaged tissue recruit polymorphonuclear cells (PMNs), which release collagenases and other proteases. These enzymes can cause corneal melting (keratolysis), typically peaking between days 7 and 21 after injury, a phenomenon sometimes called the "sterile ulceration" phase. This is why steroid use after day 10 to 14 is controversial, as steroids inhibit collagen synthesis and may worsen corneal thinning during this vulnerable window.

2. Classification and Clinical Manifestation

The Roper-Hall classification (modified Hughes classification) is the most commonly tested grading system. It guides both prognosis and management.

Roper-Hall Classification

Grade	Corneal Findings	Limbal Ischemia	Prognosis
I	Corneal epithelial damage only, cornea is clear	No limbal ischemia (0 clock hours)	Excellent; full recovery expected
II	Corneal haze present but iris details still visible	Less than one-third of limbus involved (less than 4 clock hours)	Good prognosis
III	Total corneal epithelial loss; stromal haze obscures iris details	One-third to one-half of limbus involved (4 to 6 clock hours)	Guarded; significant risk of permanent visual impairment
IV	Cornea is opaque (porcelain white); no view of iris or pupil	More than one-half of limbus involved (more than 6 clock hours)	Poor; high risk of corneal perforation, stem cell failure, and permanent blindness

Dua Classification

Grade	Limbal Involvement (Clock Hours)	Conjunctival Involvement (%)	Prognosis
I	0	0%	Very good
II	Less than or equal to 3	Less than or equal to 30%	Good
III	Between 3 and 6	30% to 50%	Good to guarded
IV	Between 6 and 9	50% to 75%	Guarded to poor
V	Between 9 and 12	75% to less than 100%	Poor
VI	Total limbus involved (12 clock hours)	100%	Very poor

The Dua classification separates the most severe injuries into three categories (IV, V, VI) instead of grouping them all as "Grade IV," which allows for more precise prognostication. For exam purposes, Roper-Hall is more commonly referenced.

A key clinical pearl: in very severe (Grade IV) burns, the eye may appear paradoxically white and quiet because the conjunctival and episcleral blood vessels are completely destroyed. This "porcelain white eye" appearance can mislead an inexperienced examiner into underestimating the severity.

3. Diagnostic Workup

Test	Role	Key Finding
pH testing (litmus paper)	Best initial and most important test	Must be repeated after irrigation until pH is 7.0 to 7.3
Slit lamp examination	Assess corneal clarity, epithelial defects, limbal status	Grading by Roper-Hall; fluorescein staining shows epithelial loss
Fluorescein staining	Evaluate corneal epithelial integrity	Uptake indicates epithelial defect; large confluent staining suggests severe burns
Intraocular pressure (IOP)	Assess for secondary glaucoma	Elevated IOP may occur from trabecular meshwork damage or inflammation
Eversion of eyelids	Check for retained chemical particles	Particularly important in calcium hydroxide (cement/plaster) injuries where solid particles may lodge in the fornices

The single most important diagnostic and therapeutic action is immediate pH testing of the ocular surface. However, this does not mean you should delay irrigation to check pH. The correct sequence, which is heavily tested, is:

Begin copious irrigation IMMEDIATELY at the scene or upon arrival, before any other assessment including visual acuity.
After a minimum of 15 to 30 minutes of continuous irrigation (using at least 1 to 2 liters of fluid), recheck pH.
If pH has not returned to the range of 7.0 to 7.3, continue irrigation and recheck every 5 to 10 minutes.
Only after pH has normalized do you proceed to a formal slit lamp examination and clinical grading.

Irrigation should be performed with isotonic saline or lactated Ringer's solution if available. If neither is available, any clean water source is acceptable. The key principle is that no time should be wasted looking for the perfect irrigation fluid. A Morgan lens (a scleral contact lens connected to IV tubing) can facilitate continuous, hands-free irrigation.

During eyelid eversion, look for and remove any retained particulate matter, especially in burns from cement, plaster, or calcium hydroxide. Retained solid particles act as a continuous reservoir of alkali and will continue to damage tissue even during irrigation.

4. Management and Treatment

Phase	Intervention	Details
Immediate (field/ED)	Copious irrigation	Start BEFORE anything else; use saline, LR, or clean water; irrigate for at least 30 minutes; goal pH 7.0 to 7.3
Immediate (field/ED)	Remove particulate matter	Evert lids, sweep fornices with moistened cotton swab
Acute (post-irrigation)	Topical antibiotics	Erythromycin ointment or fluoroquinolone drops (e.g., moxifloxacin 0.5%) four times daily to prevent secondary infection
Acute	Cycloplegic agent	Cyclopentolate 1% or atropine 1% two to three times daily for pain relief (reduces ciliary spasm) and prevents posterior synechiae
Acute	Topical ascorbic acid (Vitamin C)	10% ascorbic acid drops, every 1 to 2 hours; promotes collagen synthesis and counters the collagenase activity that causes corneal melting
Acute	Oral ascorbic acid	2 grams orally four times daily (total 8 g/day) as adjunct to topical ascorbate
Acute	Topical citric acid (sodium citrate 10%)**	Every 2 hours; chelates calcium and inhibits PMN-derived collagenase
Acute	Topical corticosteroids	Prednisolone acetate 1%, every 1 to 2 hours for the first 7 to 10 days ONLY; helps reduce acute inflammation
Acute	IOP-lowering agents	Topical timolol 0.5% or oral acetazolamide if intraocular pressure is elevated
Chronic/Surgical	Amniotic membrane transplant	For persistent epithelial defects in Grade III to IV injuries
Chronic/Surgical	Limbal stem cell transplant	For limbal stem cell deficiency with conjunctivalization
Chronic/Surgical	Penetrating keratoplasty (corneal transplant)	For end-stage corneal opacification after the ocular surface has been stabilized

Irrigation is the cornerstone and must begin within seconds of exposure. Every minute of delay increases the depth and severity of injury. The exam will test whether you recognize that irrigation takes priority over visual acuity, slit lamp exam, or even history taking. A vignette might describe a chemical splash and then ask "What is the next best step?" The answer is always irrigation, regardless of what other information is offered or requested.

Topical steroids are used aggressively during the first 7 to 10 days to suppress the neutrophilic inflammatory response. However, after day 10 to 14, steroids should be tapered and discontinued because they inhibit fibroblast collagen synthesis. The period from day 7 to 21 is when collagenase-mediated corneal melting is at its peak. Using steroids during this window accelerates stromal thinning and raises the risk of corneal perforation. This "steroid controversy" is a high-yield exam topic.

Ascorbic acid (both topical and oral) is a cofactor for collagen synthesis and helps restore the depleted ascorbate levels in the aqueous humor following alkali injury. It directly counteracts the collagenase-mediated destruction and promotes stromal repair.

Citric acid (sodium citrate 10%) works by chelating calcium ions, which are required by PMN-derived collagenases (matrix metalloproteinases) to function. By removing calcium, citrate effectively inhibits the enzymes responsible for corneal melting.

For Grade III and IV injuries, early referral to an ophthalmologist or corneal specialist is essential. These patients may require amniotic membrane transplantation to provide a biological scaffold for epithelial healing, followed later by limbal stem cell transplantation and eventually corneal transplantation if corneal opacity persists.

Contraindications and cautions:

Do NOT use steroid drops beyond 10 to 14 days without ophthalmology guidance due to the risk of corneal melting and perforation.
Do NOT patch the eye, as this retains heat and prevents monitoring.
Do NOT attempt to neutralize the chemical with another chemical (e.g., using acid to neutralize alkali). The exothermic reaction will cause additional thermal injury.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Thermal burn of the eye	Both present with acute eye pain, tearing, and corneal damage after an exposure event	Thermal burns typically cause lid burns and singed lashes; no pH abnormality on litmus testing; history involves heat/flame rather than chemical splash
Ultraviolet keratitis (welder's flash / snow blindness)	Acute bilateral eye pain, tearing, photophobia, and foreign body sensation	Onset is delayed 6 to 12 hours after UV exposure; punctate epithelial erosions on slit lamp; history of welding or tanning bed without eye protection; pH is normal
Acute angle-closure glaucoma	Severe eye pain, blurred vision, and red eye	Presents with mid-dilated, fixed pupil, halos around lights, nausea/vomiting; no history of chemical exposure; corneal edema is from elevated IOP rather than chemical destruction
Bacterial keratitis (corneal ulcer)	Painful red eye with corneal opacity and epithelial defect	Usually has a preceding history of contact lens wear or corneal abrasion; slit lamp shows a focal infiltrate with surrounding stromal haze; no chemical exposure history
Anterior uveitis (iritis)	Eye pain, photophobia, and tearing	Shows cells and flare in the anterior chamber on slit lamp; ciliary flush pattern; consensual photophobia (pain when light is shone in the opposite eye); no chemical exposure
Allergic conjunctivitis	Chemosis (conjunctival swelling), tearing, redness	Dominated by itching as the primary symptom; bilateral; papillae on tarsal conjunctiva; no corneal opacification or limbal ischemia

6. Traps and High-Yield Pearls

The most common way students get questions about chemical eye injuries wrong is by delaying irrigation to perform another step first. The exam will tempt you with answer choices like "check visual acuity," "perform a slit lamp examination," "obtain a detailed history of the chemical involved," or "instill topical anesthetic before irrigation." While topical anesthetic may help the patient tolerate irrigation, the correct answer to "What is the FIRST step?" is always begin copious irrigation immediately. Nothing takes priority over irrigation, not even identifying the chemical agent.

The second major trap involves the porcelain white eye. A vignette describing a completely white, painless eye after chemical exposure is testing whether you recognize a Grade IV injury. Students frequently misidentify this as a "mild" injury because the eye appears calm and non-injected. The absence of redness is not reassuring; it reflects total vascular obliteration and carries the worst prognosis.

The third trap is the steroid timing question. A vignette may describe a patient on day 14 after a chemical burn who is developing progressive corneal thinning, and ask you to identify the cause or next step. The answer hinges on recognizing that continued steroid use beyond 10 to 14 days contributes to corneal melting, and steroids should be tapered.

Finally, remember that alkali is always worse than acid (except hydrofluoric acid). If a vignette gives you a choice between two patients with similar exposure durations but one had an alkali exposure and the other acid, the alkali patient will have the more severe injury. The underlying concept being tested is the difference between liquefactive necrosis (penetrating, progressive) and coagulative necrosis (self-limiting, barrier-forming).

1d:["$","$L2c",null,{"article":{"id":"55b9490f-a470-4801-88dc-562571d71ff0","title":"Trauma Kimia Mata","content":"$2d","category":"Oftalmologi","created_at":"2026-09-05T10:15:11.512941+00:00","status":"published","subcategory":null},"questionCount":3,"sections":[{"id":"section-pathophysiology","num":"01","title":"Pathophysiology"},{"id":"section-classification-and-clinical-manifestation","num":"02","title":"Classification and Clinical Manifestation"},{"id":"section-diagnostic-workup","num":"03","title":"Diagnostic Workup"},{"id":"section-management-and-treatment","num":"04","title":"Management and Treatment"},{"id":"section-differential-diagnosis-and-distractors","num":"05","title":"Differential Diagnosis and Distractors"},{"id":"section-traps-and-high-yield-pearls","num":"06","title":"Traps and High-Yield Pearls"}],"hasSummaryTable":true}]