​Kembara Xtra - Medicine - Ocular Chemical Burns

​Kembara Xtra - Medicine -  Ocular Chemical Burns 
Chemical exposure to the eye is one of the true emergencies in ophthalmology since it can cause immediate, severe, and irreversible damage.
Burns from alkali are more severe. Alkaline substances are lipophilic and quickly penetrate eye tissue; saponification of cell membranes causes necrosis and can cause damage to the iris, cornea, sclera, lids, conjunctiva, and lens (cataracts).
- Burns from acid Since the accompanying anion of an acid denaturates proteins, interior structures are typically protected from harm (hydrofluoric acid is an exception to this rule; see below). Usually, just the cornea, conjunctiva, and eyelids are damaged.
System(s) impacted: exocrine, nervous Alternative name(s): chemical eye injuries

Epidemiology 
 Predominant sex: male > female Predominant age: can occur at any age, peaking from 20 to 40 years of age
Alkali burns are twice as prevalent as acid burns, with an estimated incidence of 300/100,000 per year. Chemical burns account for 11.5-22.1% of all ocular injuries.

Pathophysiology and Etiology 

Alkaline compounds are lipophilic substances that dissociate into cations and hydroxide after penetrating deep structures. -
Fat acids in cell membranes are saponified by hydrogen peroxide, which results in cell death.
- The cation hydrates glycosaminoglycans, which produces corneal opacification, and collagen, which causes rapid shortening and thickening of collagen fibrils. This causes an abrupt increase in intraocular pressure (IOP), which is a result of the cornea and sclera contracting and shrinking.
- The deposition of inflammatory debris within the trabecular meshwork may lead to a long-term rise in IOP.
- Deep structural penetration may also have an impact on the perfusing arteries, causing ischemia in the affected area.
Acidic substances - An anion causes protein denaturation and the creation of a protective barrier via coagulation necrosis, generating an eschar.
This less serious mechanism of injury has more obvious scarring, which could impair vision: The exception is hydrofluoric acid. It behaves like an alkaline material in its nonionized state, capable of entering the corneal stroma and causing significant anterior segment lesions. It can become ionized and join with intracellular calcium and magnesium to create insoluble complexes, which can cause potassium ion movements and cell death. Once absorbed into the system, severe hypocalcemia can happen.

Risk factors include: alcoholism; industrial work, including work in industrial chemical laboratories; construction work (plaster, cement, whitewash); cleaning agent use (drain cleaners, ammonia); automobile battery explosions (sulfuric acid); and any risk factor for assault (10% of injuries are the result of intentional assault).

Prevention includes using protective eyewear and training in proper handling of occupational exposures.

Accompanying Conditions 

Skin burns on the face, especially the eyelids, caused by chemicals or heat


Alkali burns can have initial pain that later lessens. Mild burns: pain and blurred vision. Moderate to severe burns: severe pain and markedly reduced vision. Diagnosis: Pain, photophobia, blurred vision, and a foreign body sensation. Chemical involved. Duration of exposure. Velocity of impact.

clinical assessment 

Alkaline substances can cause corneal opacification due to glycosaminoglycan hydration, however severe acid burns can also cause this symptom.
Acidic substance may have a ground-glass look due to the creation of superficial scars.
Mild burns; blurry vision; erythema and edema of the eyelids; superficial punctate keratitis or defects in the cornea; and hemorrhages without perilimbal ischemia in the conjunctiva. - Minimal anterior chamber response
 Marked conjunctival chemosis and perilimbal blanching Moderate anterior chamber reaction Increased IOP Local necrotic retinopathy Moderate to severe burns Decreased visual acuity Second- and third-degree burns of the eyelid skin Corneal edema and opacification Corneal epithelial defects 


Differential diagnoses include: thermal burns, ocular cicatricial pemphigoid, infected keratitis, ultraviolet radiation keratitis, foreign bodies, acute angle glaucoma, conjunctivitis, and conjunctivitis.

Laboratory Results 
Not essential unless a foreign body in the orbit or intraocular cavity is suspected. MRI is not advised in this situation; CT should be used instead.

Other/Diagnostic Procedures
Calculate the pH of the tear film using electronic probing or litmus paper: - Irrigating fluid with an acidic pH (normal saline has a pH of 4.5, for example) may change the outcomes.
 Thorough slit-lamp examination, fundus ophthalmoscopy, tonometry, and visual acuity testing Alkali burns may not show their full level of damage for 48 to 72 hours following exposure.

Conjunctival chemosis, hyperemia, and hemorrhages; Corneal neurotrophic keratopathy; Corneal epithelial defects or superficial punctate keratitis, edema, or opacification; Perilimbal ischemia; Anterior chamber response; Increased IOP


Management 
In order to reduce long-term consequences, thorough irrigation and removal of corneal or conjunctival foreign bodies are always the first line of treatment:
Passively open the patient's eyelid, and while irrigating, have them stare in all directions.
Make sure to use lid eversion to flush out all chemical reservoirs from the eyes.
Continue irrigation until the tear film and superior/inferior cul-de-sac are stable and have a neutral pH (7.2 0.1): - Irrigation should continue while being transported to the hospital for severe burns for at least 15 to 30 minutes and up to 2 to 4 hours.
- Polymethylmethacrylate scleral lenses, also known as Morgan lenses, are a good approach to achieve continuous irrigation over an extended length of time.
Even if the patient claims to only have unilateral ocular pain or irritation, initial pH testing should be performed on both eyes to ensure that a contralateral injury is not overlooked.
Use any nontoxic liquid that is readily accessible for irrigation on the site. Sterile water, regular saline, regular saline with bicarbonate, balanced salt solution (BSS), lactated Ringer solution, Diphoterine, or Cederroth eye wash may be used in a medical setting. Even though diphoterine or cederroth eye wash has demonstrated improved patient comfort and healing, it shouldn't stop immediate discomfort if it isn't easily accessible.
To make the patient more comfortable, a topical anesthetic (such as proparacaine or tetracaine) can be used.
Conjunctival fornices should be swept once every 12 to 24 hours to avoid symblepharon development and adhesions.


First Line of Medicine
Additional therapy seeks to reduce inflammation and collagen degradation while promoting collagen production and corneal epithelial repair. Selection is based on conditions' severity and relatedness.
- Topical prophylactic antibiotics: any broad-spectrum medication (e.g., ciprofloxacin drops every four hours, bacitracin-polymyxin B ointment every four hours). To promote healing and prevent corneal ulcers, some specialists advise adding systemic tetracycline 250 mg PO every six hours, particularly its derivatives such doxycycline 100 mg PO every day (BID) .
- Carboxymethylcellulose (Refresh Plus) drops every four hours: Promotes reepithelialization, lowers risk of recurrent erosion, and improves visual rehabilitation
- Cycloplegics: cyclopentolate 1% TID or scopolamine 1/4% BID for photophobia and/or uveitis- Prednisone 20 to 60 mg PO daily for 5 to 7 days if the inflammation is severe. - Topical corticosteroids for intraocular inflammation: prednisolone 1% or equivalent q1-2h for 7 to 10 days.
By days 10 to 14, taper quickly if the epithelium is still intact:
 Corneal thinning, ulceration, and perforation are less common when vitamin C is combined with steroids.
- Topical ascorbate solution 10% q2h and 500 mg of vitamin C (ascorbic acid) per oral dose every day (QID)
- Ocular antihypertensives for IOP >30 to reduce risk of optic nerve damage: latanoprost 0.005% qhs, timolol 0.5% BID or levobunolol 0.5% BID, and/or acetazolamide 125 to 250 mg PO q6h or methazolamide 25 to 50 mg PO BID ; acetylcysteine (Mucom
- Bandage contact lens: Lenses that are hydrophilic and have a high oxygen permeability promote basement membrane regeneration and epithelial migration/adhesion.
 Safety measures
- Levobunolol and timolol: history of pulmonary/cardiovascular illness, including bradycardia, asthma, and COPD
Methazolamide with acetazolamide: a history of metabolic acidosis or nephrolithiasis Mannitol: HF, renal failure, or sickle cell history
- History of urinary retention with scopolamine
- Ascorbic acid: previous history of kidney dysfunction
- Tetracycline/doxycycline: Do not administer systemically to individuals who are pregnant or under the age of eight.
- Because iatrogenic infection can happen, topical corticosteroids should be used cautiously in the presence of injured corneal epithelium. Corticosteroid use for longer than six days may prevent healing and result in corneoscleral melt. An ophthalmologist consultation or daily follow-up is advised.
In more complex instances, think about additional therapies and referrals to corneal subspecialists.
- Biologic fluids with consultation from ophthalmology: 20% umbilical cord serum every 2 to 3 hours, 20% autologous serum every 2 to 3 hours, 20% platelet-rich plasma every 2 to 3 hours, or 30% to 50% amniotic membrane suspension every 1 to 2 hours. These include cytokines, vitamins, growth factors, and anti-inflammatory agents to treat neurotrophic ulcers, recurrent erosion syndrome, persistent epithelial abnormalities, dry eyes, and chronic discomfort.

Surgery 
The objectives of subacute treatment are glaucoma management, corneal clarity restoration, and restoration of the natural ocular surface structure.
 The following surgical options are available:
- Debridement of inflammatory debris and necrotic tissue - Tenoplasty to advance the conjunctiva and tenon and restore vascularity in severe burns Tectonic keratoplasty for acute perforation >1 mm, tissue adhesive (e.g., cyanoacrylate), limbal autograft transplantation for epithelial stem cell restoration, amniotic membrane transplantation, or umbilical cord serum drops to encourage quicker epithelial regeneration and an improvement in visual acuity.
- Conjunctival or mucosal membrane transplantation to repair severely damaged ocular surfaces Enucleation for uncomfortable, blind eyes - Corneal transplant (penetrating keratoplasty, anterior lamellar keratoplasty) -

Based on an ophthalmologic consultation, a review of therapeutic compliance, and concurrent burn injuries, admission


Follow-up patient monitoring may involve inpatient or pediatric care, depending on the severity of the ocular injury. If using mannitol or prednisone, periodic serum electrolytes should be considered.

Patient Education: Need for quick ocular irrigation with water after ocular chemical exposure; Shield at all times throughout acute care; Safety glasses;

According to the Dua categorization system, a poorer prognosis is associated with increased limbal involvement in clock hours and a higher percentage of conjunctival involvement. For mildly injured eyes, full recovery is typical.
Permanent vision loss in eyes that have been severely harmed is not unusual.

Complications include: progressive symblepharon, neurotrophic keratitis, cicatricial ectropion/entropion, orbital compartment syndrome, persistent epitheliopathy, keratoconjunctivitis sicca (dry eye), glaucoma, cataract, phthisis bulbi, blindness.

---