Episclera & Sclera PDF

Sclera ​ The sclera is divided into three layers: episclera (only vascular layer - blood supply from muscular arteries = anterior ciliary arteries), scleral stroma, lamina fusca (most posterior- affected in high myopes) ​ Develops from the neural crest and mesoderm, fully developed...

Sclera ​ The sclera is divided into three layers: episclera (only vascular layer - blood supply from muscular arteries = anterior ciliary arteries), scleral stroma, lamina fusca (most posterior- affected in high myopes) ​ Develops from the neural crest and mesoderm, fully developed until the fifth month of gestation ○​ Mesoderm forms sclera ​ Component of the sclera is primarily type I collagen (also III, IV, V, VI, VIII) ​ Scleral spur is a serves as the site of attachment of the ciliary musculature ​ ○​ Longitudinal muscles of ciliary body attach to s.s. + trabecular meshwork attachment ​ Protection of the contents of the globe & is site of attachment for the EOM’s Episclera = vessels more tortuous Conjunctiva = vessels more superficial and linear Anterior ciliary artery innervated conjunctival + episcleral vessels Episclera & sclera vascular plexus ​ Two Episcleral Plexus ○​ Superficial ​ Located in episclera ○​ Deep Plexus ​ Located just above the scleral stoma ​ Episcleritis- can irritate the conjunctiva too ○​ Superficial episcleral plexus congested ​ Scleritis ○​ Superficial and deep episcleral plexus congested ​  ​ ○​ Episcleritis = “bowing” of optic section = swelling w/ fluid in center ○​ Scleritis = dome-shaped optic section w/ “bowing” but no division = no fluid accumulation ​ Episcleritis – in specific section of eye (nasal, temporal- most common) ​ Episclera is a loose, vascularized connective tissue ○​ “the vascularized cover to sclera” ​ Approximately 1/3 of episcleritis have an underlying systemic disorder, the rest are related to trauma ​ Benign inflammation of the vascular connective tissue sheath between sclera and conjunctiva ​ In young adults; more in women* 3:1 ​ Is acute; can be unilateral or bilateral- mostly bilateral ​ Sectorial or diffuse ​ 60-70% idiopathic related to cause 30% ​ Usually self-limiting ​ Systemic non-infectious causes: ○​ Connective tissue disease ​ RA (#1 cause) ​ SLE (Systemic lupus erythematosus) ​ Ankylosing spondylitis ​ IBD  ​ Reiter’s ​ Psoriatic arthritis– patches in elbows, knees ​ Wegener ○​ Vasculitic disease ​ Polyarthritis nodosa ​ Behcet’s disease ​ Giant cell arteritis ​ Cogan’s Syndrome ​ Systemic infectious causes ○​ Bacteria gram +/- ○​ TB ○​ Syphilis ○​ Toxoplasmosis ○​ Viral: HSV, HZV ○​ Acanthamoeba ○​ Chlamydia ○​ Pseudomonas ​ Other causes ○​ Rosacea ○​ Atopy ○​ Thyroid ○​ Sarcoid ○​ Burns/injuries ○​ Gout ○​ Medications: Topiramate (commonly used for seizures, and migraines) or Pamidronate (used in hypercalcemia) ​ Nasal, nodular ​ Diffuse episcleritis (has tortuous vessels) ○​ Do not confuse w/ conjunctivitis ​ Symptoms: ○​ Acute onset of redness ○​ Mild pain upon eye movement (not muscle movement)- feel pain in anterior segment ○​ One or both eyes ○​ Hx of recurrent episodes is common ○​ No discharge ○​ Tearing ○​ ​ Diffuse episcleritis ○​ 80% ○​ Diffuse redness (still more in 1 section of the eye) and edema (flat) ○​ Engorgement of episcleral vessels, large vessels that run in a radial direction ○​ ​ Nodular episcleritis ○​ 20% ○​ Forms a “nodule” (mild elevation of the conjunctiva) composed of localized inflammatory cells and exudates ○​ ​ Signs of episcleritis ○​ Mild red”flush” to intense red ○​ No edema in sclera  ○​ If nodular, nodule moves ○​ Conjunctival vessels move and underlying red episcleral are immovable ○​ Mild to moderate tenderness over the episcleral injection area or nodule ○​ ​ Episcleritis = presents alone ○​ Test w/ cotton tip applicator: if nodule moves = superficial layer: episclera ​ Scleritis = deep! ○​ Test w/ cotton tip applicator: if nodule does not move = deeper and more painful ​ Work-up of episcleritis ○​ Phenylephrine test – 10-15 min later will blanch the superficial layer ○​ Nodule mobility test in nodular episcleritis ​ Moves with cotton tip applicator (it will move) ○​ Blanch = episcleritis ○​ Not blanch = scleritis ○​ SLE beam test ​ Scleral edema is present in scleritis but absent in episcleritis ​ Scleral edema may be viewed with a narrow-slit lamp beam (optic section/parallelepiped) after applying topical phenylephrine ​ It will manifest as “bowing” of the beam along the sclera ​ Deep scleral part of the beam not displaced ​  ​ ​ Differential dx: ○​ Scleritis = severe pain that radiates to ipsilateral side of face, no blanch to phenylephrine, nodule does not move when touched w/ cotton tip and typically presents in older patients ○​ Iritis: cells and flare in A/C; may present w/ scleritis ○​ Conjunctivitis (viral, bacterial, allergic) ​ Diffuse redness and discharge w/ follicles or papillae ○​ Phlyctenular keratoconjunctivitis ​ Plyctena near cornea ​ ○​ Anterior uveitis ​ Cells and flare ​ Hypopyon ​ Treatment/Management ○​ R/O underlying cause ​ History: previous red eye or same episode in the past ​ Patient can be using OTC drugs that cause vasoconstriction ​ ROS: if positive (+), order lab tests accordingly ​ If non-specific or recurrent: chest x-ray (if suspect TB, sarcoidosis), RF, ANA (if suspect SLE), ESR, VDRL, FTA-ABS, uric acid, among other  ​ Complete exam including DFE ○​ Mild (TID) ​ Self-limiting, artificial tears, cold soaks ​ Could use mild steroids QID (FML 0.1%) -> 1st line** ​ May resolve spontaneously in 7-10 days ​ F/U q 7 days ○​ Moderate-severe (can use Prednisolone if severe) ​ Mild steroids: FML 0.1%, Loteprednol 0.5% QID until improvement and taper ​ If no relief: (if moderate) + patient complains of pain ○​ Oral NSAID (** do NOT use topical NSAIDs such as Ketorolac as it can melt the cornea**) ​ Ibuprofen 200-600 mg TID or QID (cheapest and most common) ​ Naproxen 250-500 mg BID (Alleve) ​ Flurbiprofen 100 mg TID (Expensive for an NSAID) ○​ F/U q 3-5 days Scleritis (more severe!) ​ A severe and intense inflammatory condition w/ edema & cell infiltration to sclera ​ Inflammation can destroy collagen and thus its structure ○​ Collagen fiber melt away = reveals bluish color of uvea (choroid) ​ Deep episcleral vessels and scleral-perforating capillary and postcapillary venules provide potential inflammatory components which can lead to scleral destruction ​ 4-6 decade, > females (30-59 y/o) ​ 50-57% of cases have an identifiable underlying cause (higher in cases of necrotizing) ○​ Systemic auto-immune inflammatory diseases - RA, Wegner’s granulomatosis, SLE, Polyarteritis nodosa, IBD ○​ Infectious - syphilis, sarcoidosis, TB ○​ Local causes – herpes zoster, trauma, surgery (surgery-induced necrotizing scleritis SINS) ○​ Other – gout, erythema nodosum ​ Bilateral is more common in 50% of cases ○​ Initial presentation can be unilateral ​ In ~15% of patients, scleritis is the initial presentation of underlying connective tissue (RA) or vasculitic disease (GCA) ​ 70% of recurrence rate  ○​ Remember it is idiopathic ​ Can be the 1st sign of systemic disease ○​ *mandatory to order lab tests in scleritis ​ ​ Subtypes ○​ Subtypes of scleritis are helpful to determine prognosis, but not cause ○​ Anterior scleritis is the most common (90%) ​ Divided into ​ ○​ Posterior scleritis is an unusual form ​ Anterior: swollen sclera displaces episcleral vessels forward ○​ Non-necrotizing diffuse & nodular ○​ Diffuse: widespread inflammation of the anterior segment ○​ Nodular: immovable inflamed nodule ○​ Necrotizing w/ inflammation ​ MOST severe ​ RA patients show white avascular tissue from infarction, edema around, and uvea shows ○​ Bilateral 60% cases ○​ Extreme pain ○​ Mortality rate 25% within 5 years of onset of scleritis ○​ Visual prognosis poor ○​ ○​ Necrotizing w/o inflammation ​ Aka scleromalacia perforans ​ More common in chronic RA ​ Almost lack of symptoms ​ ○​ Symptoms of anterior scleritis ​ Usually unilateral* @ initial stages but mostly found bilateral ​ Severe, excruciating pain ​ Radiates to the forehead, brow, jaw or sinuses ​ CN V: V1 (ophthalmic), V2 (cheek), V3 (jaw) ​ Pain - awakens patient, worst upon touch, tender, temporally relieved by analgesics ​ Gradual or acute onset w/ red eye ​ Tenderness of globe ​ Photophobia (common to find WBC in anterior chamber) ​ Tearing ​ Deep bluish, violaceous hue (best seen w/ daylight) ​ Scleral vessels are larger & deep could not be moved ​ Anterior uveitis could be present (cells in AC) ​ Phenylephrine: negative blanching* ​ Positive in episcleritis ​ Anesthesia test: negative ​ Not normally done in episcleritis ​ Nodule not movable ○​ Work-up approach for anterior ​ History of previous episodes  ​ Review of systems ​ Exam w/ careful DFE ​ Non-specific lab tests: CBC, chest x-ray, RF, ANA, HLA-typing, ESR, syphilis serology ○​ Treatment for anterior (non-necrotizing) ​ Treatment of underlying disease ​ Topical steroids are questionable, can give some symptomatic relief but alone are not adequate ​ First initial treatment for anterior diffuse or nodular is oral NSAIDs (mild to moderate scleritis) ​ Ibuprofen 400-600mg qid ​ Flurbiprofen 100mg tid ​ Indomethacin 50 mg tid ​ Indomethacin SR 75 mg bid ​ If not successful with 1st NSAID, try two more before going to oral steroids (piroxicam, naproxen, tolmetin, sulindac) ​ May need a H2 receptor blocker as Famotidine or Pepsin 20 mg BID or a PPI as Omeprazole or Pantoprazole 20-40 mg to prevent GI ulcer w/ long-term NSAID tx ​ If uveitis: cycloplegic and topical steroids (eg Prednisolone) ​ F/U q 2-5 days accordingly ​ Patients unresponsive to or intolerant of Prednisolone ​ Immunosuppressive drugs ​ Methotrexate (7.5-15 mg/weekly) ​ Azathioprine (1.5-2 mg/kg/day) ​ Cyclosporine (5 mg/kg/day) nephrotoxic ○​ If necrotizing inflammatory scleritis OR non-necrotizing that do not respond to oral NSAIDs ​ Steroids PO 1 mg/kg/day in severe 1.5 mg/kg/day ○​ Prednisolone 60-100 mg/day ○​ Tapered to best tolerated dose ○​ Severe cases patients require daily prednisolone for 6 months or more ○​ Necrotizing: oral steroids like above and immunosuppressants– to avoid longterm corticosteroid effects (eg Cushing’s syndrome, osteoporosis) ○​ Scleromalacia perforans ​ Intensive lubrication ​ Scleral patch graft if risk of perforation ​ Donor sclera (Can melt away) ​ Autologous periosteum (less like to necrose) ​ Posterior: extension into choroid and retina ○​ Unseen external scleral signs w/ severe pain ○​ Internally patient may have choroidal folds, ONH and macular edema, and even exudative RD ○​ 10% of cases ○​ Symptoms: pain ○​ Involves sclera posterior to the equator ○​ May start posteriorly or may extend from an anterior scleritis ○​ ○​ Signs: ​ VA could be affected ​ Choroidal folds, choroidal detachment ​ ONH edema ​ Retinal hemorrhage ​ Exudative RD ​ Macular edema ​ Could stimulate an amelanotic choroidal mass ○​ Diagnostic tests ​ Phenylephrine test: negative ​ SLE beam test (swelling sclera) ​ Nodule movement test (-) ​ Anesthesia test (-) ​ T sign in B-scan ultrasonography ​ Choroidal folds in OCT  ​ ○​ Work-up approach for posterior ​ Fundus exam, VA, EOM, CT, B-scan ultrasound, FA ○​ Treatment ​ NSAIDs PO, steroids PO, and immunosuppressants if patient has systemic disease ○​ Ocular complications for posterior scleritis ​ Corneal involvement (37%) ​ Stromal keratitis ​ Sclerokeratitis ​ Marginal keratolysis ○​ ​ Anterior uveitis (30%) ​ Glaucoma (15%) ​ Neovascular glaucoma ​ Cataract (7%)- PSC from steroids ​ Visual loss (27-37%) ​  ○​ Prognosis ​ Mild to moderate scleritis: maintain vision ​ Necrotizing scleritis: ​ Worse prognosis than non-necrotizing disease ​ High incidence of visual loss ​ 21% - 8 year mortality ○​ Coronary arteritis or cerebral angiitis (tx aggressive immunosuppressive therapy) ​ ​ Common lab tests for scleritis ○​ ACE: Sarcoidosis (chest x-ray) ○​ ANA: Lupus ○​ c-ANA: Wegener’s granulomatosis ○​ p-ANA: Vasculitis, Polyarteritis nodosa ○​ FTA-ABS: Syphilis ○​ ELISA: Lyme disease ○​ RF: Rheumatoid arthritis ○​ ESR: Nonspecific systemic inflammation ​ If suspect CT disease Episcleritis: ​ No pain to mild ​ Infrequent systemic association ​ Movable over the sclera ​ Vision unaffected ​ Frequently resolves without treatment ​ Phenylephrine test positive ​ No complications Scleritis: ​ Mild to severe pain ​ Frequent systemic association ​ Not movable ​ Vision frequently affected ​ Requires treatment for resolution ​ Phenylephrine test negative ​ Frequent complications Scleromalacia Perforans ​ Van der Hoeve 1934 first describes it ​ Rare scleral disease (only 4% scleritis) ​ Progressive scleral thinning without inflammation ​ Change scleral color to yellow or greyish subconjunctival nodules ​ Gradually developed into scleral necrosis with perforation and exposure of the uvea ​ Lack of symptoms ​ Main characteristic: necrotizing w/o inflammation ​ ​ Necrotic slough without surrounding inflammation ​ Absorption or slough separation leaves bare uvea covered only by thin conjunctiva ​ Pathological vessels anastomosing with each other surround or cross the abnormal area (join to perilimbal vessels) ​ ​ Commonly associated w/ severe, progressive, long-standing RA ​ More frequent females ​ Other systemic vasculitic disorders ​ Histopathology ○​ Chronic granulomatous changes w/ epitheloid cells ○​ Infiltration of the scleral stroma by inflammatory cells: prolonged vaso-occlusion  ○​ Autoimmune reaction responsible of vessel damage (hypersensitivity type 3) ​ Complications ○​ Visual loss ​ Progression of astigmatism (scleral and paralimbic/corneal changes) ○​ Anterior uveitis ○​ Cataract (secondary to uveitis or steroid therapy) ○​ Glaucoma (secondary to ocular abnormalities or steroid therapy) ​ Treatment ○​ Topical NSAIDs and steroids are insufficient ○​ Immunosuppressive therapy* should give immunosuppressors for this disease ​ Cyclophosphamide – most effective drug in noninfectious necrotizing scleritis ​ Oral dose 2-3 mg/kg/d ​ Methotrexate 7.5-20 mg weekly ​ Azathioprine start 2.5 mg/kg/d ​ Cyclosporine 2.5-5 mg/kg/d ○​ “biologics” modifying immune response agents ​ Tumor necrosis factor inhibitors ​ TNF1 (etanercept, infliximab) ​ Interleukin-2 receptor blocker (daclizumab) ​ Interleukin 1 receptor antagonist (anakinra) ​ Antilymphociyte tx (rituximab, alemtuzumab) ○​ Tx with specialist ​ Surgical treatment ○​ Necessary cases with exposed uvea o preserve globe integrity ○​ Tectonic patch grafting ​ Fresh or frozen globe or glycerin preserved scleral tissue ​ Dermis ​ Fascia lata ​ Periosteum ​ Aortic tissue ​ Cartilage ​ Cornea ​ Pedicle-flaps of conjunctiva with Muller muscle or tarsus ​ Synthetic material – GoreTex ​ Amniotic membrane Hyaline Degeneration ​ Symptomless lesions ​ Patients age of 50 or more ​ Patch w/ scleral degeneration = transparent ​ Located in the interpalpebral region close to the insertion of the recti muscles ​ Area of translucent or transparent sclera (2 mm) ​ Center appears facetted surrounded by a dense yellow ring (oval in shape) ​ The center transilluminate (thickness change form 0.6mm to 0.3 mm) ​ Bilateral, symmetric, well-defined with a vertically ovoid shape ​ ​ No inflammatory process ​ Pathogenesis unknown ​ Do not become under age of 60, so probably is a degeneration of scleral collagen at the side of maximal tension of the horizontal EOMs ​ Hypothesis: ○​ Mechanical stress ○​ Actinic damage ​ Differential diagnoses ○​ Scleromalacia perforans ​ No treatment required ​ Usually no complications ​ Associated factors ○​ Female sex- menopause ○​ Degenerative arthritis ○​ Age range over 70 years ○​ Moderate to high myopia Staphyloma of the Sclera ​ Ectatic sclera (outpouching of the wall) ​ Sclera has become attached to the underlying uvea ​ Staphylos (brunch of grapes) ​ Secondary to a severe pathology in the sclera (scleritis or uveitis) ​ Chronic longstanding rise in IOP cause scleral expansion ○​ Young ○​ Chronically inflamed eyes ​ The inflammation is postequatorial ​ ​ Fusion of the uvea to the sclera with loss of choriocapillaris ​ Nutritional changes in the scleral follow ○​ Loss of scleral fibers ○​ If severe the underlying uvea and retina prolapse outwards ​ Equatorial staphyloma may form at the exit site of the vortex vein or close to the equator ○​ Fibers are more loosely arranged ​ Tx ○​ Scleral graph ○​ Manage complications (RD) ​ ​ Anterior staphyloma ○​ Anterior to the equator ​ Calary - over the ciliary body ​ ​ Intercalary – involving the limbus ​  ○​ Pathogenesis: after inflammation in the sclera and only if the IOP is very high (40mmHg) ○​ Patients with chronic anterior uveitis with massive anterior synechiae and secondary glaucoma ○​ Nutrition of iris and sclera is disturbed ○​ Peripheral retina degenerate, also retinal tears can appear ​ Posterior staphyloma ○​ Posterior part of the sclera possibly including the disc bulge outwards ○​ Pathology: ​ Result of pathologic myopia* ​ Inflammatory scleral disease ​ Long standing closed-angle glaucoma ○​ Blue eye ​ Structural changes in scleral collagen fibers and thinning of the sclera allow underlying uveal pigment to be seen ​ Scleral has a bluish discoloration ​ Blue scleras also occur in several connective tissue diseases (THIN SCLERAS) ○​ Osteogenesis imperfecta ○​ Ehlers-Danlos syndrome ○​ Marfan’s syndrome ○​ Pseudoxantoma elasticum ​ Osteogenesis Imperfecta ​ “Brittle-bone disease”, genetic disease; progressive disease ​ Inherited condition that involves the skeleton, ear, joints, teeth ,skin and eyes ​ Four types of Osteogenesis ○​ Type I – autosomal dominant (blue sclera +) more common ○​ Type II – Recessive dominant (dark blue sclera ++) More aggressive ○​ Type III – Heterogeneous (variable) ○​ Type IV- Heterogeneous (less common) ​ Types III and IV the blue sclera fades with age, normal color by adolescence or adulthood ​ Abnormalities of the type I collagen gene ​ Main signs: ○​ Blue sclera ○​ Deafness ○​ Bone fractures ○​ Deformed teeth Ehlers-Danlos Syndrome ​ Defect on the cross-linking of collagen (V, I ) become weaken ​ Type VI is the one associated to ocular disease ​ Lysyl hydroxylase deficiency (enzyme necessary for collagen synthesis) ​ Signs: ○​ Hypermobile joints ○​ Fragile and elastic skin ○​ Tendency to bleed ​ Findings ○​ Microcornea or megalocornea ○​ Extreme thinning of the cornea and sclera ○​ Keratoconus, dislocation of the lens ○​ Cataract ○​ Retinal detachment ​ Scleral thinning occur in 7% of the patients ​ Rupture commonly occur Pseudoxanthoma Elasticum ​ Also known as Gronblad-Strandberg syndrome ​ Caused by an autosomal recessive mutation in the ABCC6 gene on chromosome 16p13.1 ​ Results in a fragmentation and mineralization of elastic-containing fibers in connective tissue  ​ Small, yellowish papular lesions form and cutaneous laxity mainly affects the neck, axilla, groin, and flexural creases ​ Eye findings are present in almost all PXE patients, and usually noticed a few years after the onset of cutaneous lesions ​ Gastrointestinal and cardiovascular systems may also be affected ​ Angioid steaks (breaks sclera) ○​ Named because of their resemblance to blood vessels ○​ Result from crack-like breaks in weakened Bruch’s membrane (“peau d’orange appearance) that radiate out from the optic nerve ​ Associated optic disc drusen are common ​ Usually asymptomatic Nanophthalmos ​ Bilateral inherited condition ○​ Both autosomal dominant and recessive forms ​ Characteristics: ○​ Narrow palpebral fissures ○​ Small orbit ○​ Short axial length eye (14-20 mm) ○​ Hyperopic patients (+10 - +20) ○​ Normal or reduced corneal diameter ○​ Normal-sized crystalline lens ○​ Thick sclera (high collagen bundles and increased glycosaminoglycan's) ​ Associated to ○​ Mucopolysaccharidosis (abscense of glycosaminoglicans) ○​ Fetal alcohol syndrome ○​ Myotonic dystrophy ○​ Achondroplasia (dwarfism without cartilage formation) ​ Aging nanophtlamic sclera becomes less elastic and may result in increased resistance to venous outflow through the vortex veins ​ Lead to choroidal congestion, thickening and eventually effusion ○​ can occur spontaneously or after decompression of the eye in a surgery for cataract or glaucoma ​ Other complications risks during intraocular surgeries ○​ Cystoid macular edema ○​ ERD (exudative retinal detachment) ○​ Malignant glaucoma ○​ Vitreous hemorrhage Scleral injury: trauma ​ Orbit protects form injury the sclera ​ Sclera stand high pressures if is applied slowly ​ 40-60% of the eyeball radius has to be indented before rupture ​ Ruptures result from direct sharp injury or are consequence of a large blunt object striking the eye obliquely ​ Axial blows rarely ruptures the sclera ​ Scleral rupture after blunt trauma is often difficult to diagnose ​ Rupture follows the circumferential pattern of the anterior scleral fibers ​ Extends form the limbus backwards ​ Scleral dehiscence usually is 10-14 mm ​ Scleral rupture is usually accompanied by ○​ Subconjunctival hemorrhage ○​ Intraocular hemorrhage ○​ Low vision (PL or HM) ○​ Low IOP ​ Scleral rupture is common during retinal detachment surgery ○​ Thin wall myopic eyes ○​ Re-operations after cryotherapy ​ Treatment ○​ Closure of the rupture ○​ Manage complications Scleral injury: foreign bodies ​ Most common high velocity foreign bodies penetration ○​ Often transverse ​ Lower velocity foreign bodies ○​ Explosions ​ Embed material into the sclera where usually not harm ​ Removal only indicated if the patient has discomfort (cyst of the epithelium of the conjunctiva can occur) ​ Diagnosis ○​ Clinical ○​ X-ray ○​ CT-scan only if its necessary ○​ MRI contraindicated in metal FB Sclera injury: chemical injury ​ Frequent but rarely involve scleral tissue ​ Chemical can be introduced in  ○​ Solid form as dust or larger particles: prolonged contact so more potential damage ○​ Liquid or vapors: rapidly removed by the tear reflex production ​ Most common ○​ Cosmetics, disinfectants ○​ Detergents ​ Cationic are very corrosive in high concentrations ○​ Fertilizers and pesticides ○​ Car batteries (dioxide and sulfuric acid) ​ Acid burns ○​ Acid with a pH below 2.5 cause a considerable damage ○​ Coagulation, denaturation and precipitation of the proteins of the sclera ​ Destruction of cellular content ○​ Organic and inorganic acid similar action ​ Dissociate in water to form hydrogen ions ​ Inorganic acids lower pH- more damage ​ Sulphurous acid penetrated more rapidly than hydrochloric, phosphoric or sulfuric acids ○​ Sulfuric acid content in car batteries - most common cause ​ Alkali burns ○​ Damage depends on the length of time the alkali is in contact with the surface and the pH of the substance ○​ Higher pH more damaging ○​ More common ​ Ammonia ​ Sodium hydroxide (caustic soda or lye) ​ Calcium hydroxide (cements) ○​ Damage of the tissue through saponification of the fatty acids within cell membranes ​ Cell destruction ​ Loss of cellular adhesion ​ Softening and gelatinization of the tissue ​ NECROSIS ○​ Intense immunological reaction ○​ Limbal ischemia ○​ Alkali is the major ocular emergency ○​ Worse than acid burn