Thermal Injuries to the Eye : Introduction, Symptoms, Causes, Diagnosis, Management and Prevention - www.genericdrugscan.com

Thermal Injuries to the Eye : Information

Thermal injuries to the eye are potentially blinding eye injuries and constitute true emergencies. Thermal injuries to the eye are less common than chemical injuries, with very different forms of ocular insult, post-injury problems, and treatment approaches.

Thermal injuries are of importance due to increased occurrence during festival and festivities.

Thermal injuries and Festival/ Festivity in India:

Diwali (Deepavali): Diwali is an important Indian festival celebrated by lighting lamps and bursting crackers. Diwali festival also marks end of month Ashwin and beginning of Kartik month of Indian calendar, and it falls in the month of October or November every year.

Firecrackers are extensively used during festivals and festivities in India. Fireworks are used during celebrations because of sound produced, sparkle and sudden burst of colours. Whenever firecrackers are used, there is always a risk of burn and injury. Crackers also cause noise/ air pollution and may aggravate systemic diseases like bronchial asthma.

The chemicals released by the firecrackers are also harmful. Chemicals in fireworks include sulphur dioxide, lead, cadmium, copper, magnesium, nitrate and nitrite.

Firecrackers release chemical pollutants such as carbon dioxide and carbon monoxide.

Magnesium hydroxide is found in sparklers and flares; the combination of thermal injury and chemical injury accounts for more severe injury than that being produced by either type alone.

Facial burns are a frequent component of thermal injury and ocular involvement may be a part of it in some patients. The lids, especially the margins, are selectively protected from burns. This is because protractor spasm causes orbital and preseptal tissue to overlap and cover the tarsal region. The incidence of lid involvement is increased with more extensive burns. This is especially true when patients are unconscious secondary to an explosion or smoke inhalation and the protective reflexes are not intact. Fortunately, thermal injury is not commonly associated with severe ocular sequelae, courtesy of inherent protective mechanism, such as blink reflex, Bells phenomenon, and reflex shielding movements of the head and arms. The loss of an eye primarily from thermal trauma is uncommon and the risk of permanent visual impairment can be minimised with effective timely treatment. Involvement of the eyelids and lid margins is the most frequent ophthalmic manifestation. With thermal injury, eyelid damage leads to necrosis of tissues, eschar formation, and, finally, quantitative loss of tissue. Therefore, the eyelid and conjunctival support system of the cornea is compromised, further embarrassing any corneal or anterior segment pathology. Chronic exposure keratitis is one of the greatest threats to corneal integrity and visual rehabilitation. However, ocular trauma may occur in the absence of eyelid injury and all patients who have been exposed to fumes, heat and smoke warrant comprehensive eye examination.

Direct thermal damage to the cornea produces collagen shrinkage, with prominent stress lines radiating away from the area of greatest injury, especially in case of hot metal contact to the surface. This shrinkage might be severe enough to make the cornea distorted and opaque, leading to steepening of the axis of severest injury. Collagen damage may be so severe as to produce a rapidly excavating corneal ulcer originating from liquefactive necrosis. The post-injury phases of thermal injuries have not been studied as comprehensively as chemical injuries.

When both thermal and chemical injuries occur simultaneously, the terms thermal-alkali injury or alkali-thermal injury might be used, with the most prominent injurious agent stated first. Thermal injuries associated with acid injuries may be referred to in a similar way.

References:

Holland Edward J, Mannis Mark J, Lee W Barry. Ocular Surface Disease - Cornea, Conjunctiva and Tear Film. Elsevier Saunders. 2013. P. 219- 230

Roy Frederick Hampton, Tindall Renee. Master Techniques in Ophthalmic Surgery. Second Edition. Jaypee Brothers Medical Publishers (P) Ltd 2015. P 114- 120.

Black Evan H, Nesi Frank A, Gladstone Geoffrey J, Levine Mark R. Smith and Nesis Ophthalmic Plastic and Reconstructive Surgery. Third Edition. Springer 2012. P 229- 235.

Heegard Steffen, Grossniklaus Hans. Eye Pathology- An illustrated guide. Springer- Verlag 2015. P 46- 49.

Gold Daniel H, Lewis Richard Alan. Clinical Eye Atlas.Second Edition. Oxford University Press. 2011. P. 225- 229.

Benitez-del-Castillo Jose M. Lemp Michael A. Ocular Surface Disorders. JP Medical Ltd, Victoria Street, London, SW1H 0HW, UK. 2013. P. 149-156.

Holland Edward J, Mannis Mark J. Ocular Surface Disease- Medical and Surgical Management. Springer- Verlag New York 2002. P 100- 111.

http://bjo.bmj.com/content/85/11/1379.full

http://emedicine.medscape.com/article/798696-overview

http://eyewiki.aao.org/Eyelid_Burns

http://onlinelibrary.wiley.com/doi/10.1034/j.1600-0420.2002.800102.x/pdf

http://www.oftalmo.com/seo/archivos/maquetas/A/5BFBFF11-C25C-4249-B32D-00001FE1F6DA/articulo.html

http://www.ijburns.com/article.aspissn=0971-653X;year=2014;volume=22;issue=1;spage=22;epage=32;aulast=Sarabahi

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC421790

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3385409

http://www.diwalifestival.org/environmentally-safe-diwali.html

http://www.worldofchemicals.com/media/diwali-festival-of-light-not-pollution/7701.html

Hughes WF Jr. A. Alkali burns of the eye. II. Clinical and pathologic course. Arch Ophthalmol 1946; 36: 189- 214.

Jackson DM. The diagnosis of the depth of burning. Br J Surg 1953; 40: 588- 596.

Ballen PH. Mucous membrane grafts in chemical (lye) burns. Am J Ophthalmol 1963; 55: 302- 312.

Roper- Hall MJ. Thermal and Chemical burns. Trans Ophthalmolo Soc UK 1965; 85: 631- 653.

Goldblatt WS, Finger PT, Perry HD, et al. Hyperthermic treatment of rabbit corneas. Invest Ophthalmol Vis Sci 1989; 30: 1778- 1783.

Dua HS, King AJ, Joseph A. A new classification of ocular surface burns. The British Journal of Ophthalmology 2001; 85 (11): 1379- 1383.

Nema HV, Nema Nitin. Textbook of Ophthalmology. Fifth Edition. Jaypee Brothers Medical Publishers (P) Ltd. 2008. P 360.

Yanoff Myron, Sassani Joseph W. Ocular Pathology. Sixth Edition. Mosby Elsevier 2009. P 152.

Symptoms may include:

• Severe pain.
• Red eyes.
• Watering or epiphora.
• Foreign body sensation.
• Blurring of vision.
• Reduced visual acuity.
• Photophobia (increased sensitivity to light).
• Blepharospasm.

In massive thermal burns, patient may require systemic resuscitation.

Thermal injuries result from accidents associated with firework explosion, steam, boiling water, or molten metal. Thermal burns include those caused by a flame, which are usually severe with deep tissue injury, and those caused by flash accidents, such as explosions or electrical arcs, which are usually more superficial but may be extensive. The thermal injury is immediate and non-progressive.

The majority of ocular thermal injuries can be divided into:

• Flame burns: Flame burns are secondary to fire. They tend to be deep dermal or full thickness.
• Scalds: Scalds may be caused by spilling hot drinks or liquids or being exposed to hot bathing water. Scalds tend to cause superficial to superficial dermal burns.
• Contact burns: Contact burns are the result of direct exposure to a hot object. Contact burns tend to be deep dermal or full thickness.

The severity of burns depends upon the intensity of the burning agent, both the quantity of heat transmitted by the burning agent and amount of the burning agent, the duration of exposure, use of protective device, body response, any first aid or irrigation of the affected eye.

Most of the flash burns are superficial but may be extensive. In burns due to flames, the period of exposure is longer and it results in deep burns.

Liquid thermal burns vary in severity depending on the substance. Injury due to steam and also due to explosion of liquids on removal from microwave may splash into the eye and cause burns. The temperature of non- combustible liquid like water is usually less on body contact, and such liquids dissipate rapidly from the initial contact area, thereby causing superficial burns only. The temperature of combustible liquids (e.g. petrol), is usually high on contact with the body. These liquids are more viscous and may burn the clothes as well. Therefore, the damage is more localised but may be deep.

Pathophysiology:

Eyelid injury:

The skin is made up of two layers:

• Superficial epidermis.
• Deeper thicker dermal layer.

These layers cover the subcutaneous tissues and a deeper muscular layer.

Jackson (1953) described three zones of burn:

• Zone of coagulation: Zone of coagulation occurs at the point of maximum damage. There is irreversible tissue loss due to coagulation of the constituent proteins. Tissue in this zone must be d brided. The zone of coagulation is surrounded by the zone of stasis.
• Zone of stasis: The surrounding zone of stasis is characterised by decreased tissue perfusion due to vasoconstriction and ischaemia. The tissue in this zone is potentially salvageable. The zone of stasis is surrounded by zone of hyperaemia.
• Zone of hyperaemia: In this outermost zone of hyperaemia, tissue perfusion is increased due to vasodilatation. The tissue in this zone typically remains viable. The tissue here invariably recovers unless there is severe sepsis or prolonged hypo-perfusion.

These three zones of burn are three dimensional, and loss of tissue in the zone of stasis will lead to the wound deepening as well as widening.

Healing process of eyelid thermal injuries:

Re-epithelialisation of wounds occurs from epithelium located at wound edges and skin appendages. In large epithelial defects, granulation tissue bridges the wound before epithelialisation. Wound contraction takes place in second- and third-degree burns and aids in restoring epithelial continuity. The property of wound contraction distorts the eyelids and hampers their function. Owing to the thinness of skin and absence of subcutaneous fat and rich blood supply, the slough on the lid separates early. The raw surface needs to be grafted, if contraction of wound is to be avoided.

Adjacent soft tissue injuries (e.g. cheek, forehead): In adjacent soft tissue injuries, skin contraction displaces the eyelids which might pull the canthus. Injuries affecting lower lid tends to be more severe, due to less available loose skin.

Thermal ocular injury:

The severity of thermal ocular injury is a function of the thermal dose and the surface area of contact. A thermal dose can be defined by a time-temperature relationship. Goldblatt et al. explored the limits of thermal tolerance in animal models, by applying well-defined heat doses (time x temperature) and examined the effects on the tissue. They found that a heat dose of 45 celsius resulted in no perceptible damage to the cornea when applied for 15 minutes, and produced mild transient stromal oedema only when applied for 45 minutes.

Higher thermal exposure produced damage with total destruction of cellular elements, massive oedema and stromal disorganisation at a temperature of 59 celsius for 45 minutes. This degree of thermal exposure resulted in severe degeneration of all structures and total necrosis at one week.

• Thermal injuries to the conjunctiva may be iatrogenic sometimes e.g. after the use of triple freeze- thaw technique during removal of conjunctival tumours. Thermal response includes:

- Initial phase: Initial phase comprises of tissue destruction.

- An interval reactive phase.

- Period of tissue repair.

Minor thermal injuries are typically limited to the conjunctival epithelium. Migration of peripheral epithelial cells then heals the ulceration with no scarring. Deeper injuries involve the stromal connective tissue and may cause coagulation necrosis. The healing process is prolonged and may result in significant scarring.

Aberrant wound healing may result in a vascularised, hypertrophic scar that mimics a pterygium, but it usually lacks the stromal elastosis as seen in pterygium. This scar may encroach on the corneal surface like a pterygium.

Excessive wound healing may also result in a so-called pyogenic granuloma. This rapidly growing and protruding lesion is histologically defined by vascularised, oedematous granulation tissue with abundance of inflammatory cells.

The lining epithelium may be eroded, and pyogenic granuloma may bleed intermittently.

• In thermal injuries to the cornea, actual burn to the surface is rare, but the injury is usually secondary to exposure, drying, and infection due to deep eyelid burns and is, therefore, preventable. In severe thermal burns, there is corneal opacification associated with extensive and deep damage to the tissues. Direct thermal damage to the cornea produces collagen shrinkage, with prominent stress lines. This shrinkage might be severe enough to make the cornea distorted, leading to steepening of the axis of severest injury. Collagen damage may be so severe as to produce a rapidly excavating corneal ulcer originating from liquefactive necrosis. Globe rupture is seen in extreme cases.]

Patients with ocular thermal trauma should undergo early evaluation of the eye to assess the extent of the injury and exclude the possibility of an intraocular or intraorbital foreign body. The frequency of eye examination must balance the risk of ocular sequelae with the risk of contamination.

Diagnosis requires:

Examination of eyelids and adjacent tissues:

• The depth and extent of burns in the eyelids and adjacent areas should be assessed initially.
• The presence or absence of eyebrow hair and eyelashes should be well documented. Presence of these indicates sparing of the eyelid margin. Loss of these is associated with a deep partial-thickness or full-thickness burn.
• Bell s phenomenon: Bell s phenomenon is a protective reflex in which eyeball is seen turned upwards and slightly outwards during eyelid closure to avoid corneal exposure. The presence or absence of Bell s phenomenon should be documented. In the presence of a partial- thickness burn, eyelid contracture produces progressive lagophthalmos (inability to close the eyelids completely) and corneal exposure. A good Bell s phenomenon may help prevent a corneal epithelial defect even in the presence of significant lagophthalmos. Absence of Bell s phenomenon may cause increased conjunctival redness, chemosis, corneal exposure, or mucous discharge and needs prompt surgery.
• Foreign bodies, if any.

Burns are categorised into degrees depending on the depth and extent of injury.

Degrees of burns:

• Epidermal burns (First-degree burns): Epidermal burns (First-degree burns) involve the epidermis. First-degree burn usually does not produce any deformity. Pain is due to local vasodilator prostaglandins, and healing is usually complete within a week.
• Partial-thickness burns (Second-degree burns): Partial-thickness burns (Second-degree burns) include injury to the dermis, formation of blisters, and swelling. There is subcuticular or dermal fibrosis with sparing of orbicularis oculi muscle fibers. Partial-thickness burns are commonly divided into superficial and deep.

Superficial partial-thickness burns affect epidermis and superficial dermis and results in thin-walled, fluid-filled blisters with a moist red base. The exposure of superficial nerves makes these injuries painful. Burn usually heals spontaneously within two weeks without significant scarring or with minimal scarring only.

Deep partial-thickness burns have a pale white or mottled base beneath the blisters. Healing takes three or more weeks, and is accompanied by scarring and contraction. Deeper second-degree burn leads to scar formation and contracture of wound, producing ectropion. These often necessitate early surgery for contraction and eyelid retraction.

• Full-thickness burns (Third-degree burns): Full- thickness burns (Third-degree burns) destroy epidermis, dermis, and all regenerative elements. There may be involvement of deeper structures as well. The skin is dry, leathery, and affected tissue is avascular and white. In the lids this appearance may be followed by oedema of the underlying tissues. The wound heals from the edges by eschar formation, followed by proliferation of granulation tissue and marked wound contraction, which may cause more severe ectropion and lid shortening. Such burns are typically painless due to loss of sensation in the involved area. Early excision of the affected tissue and skin grafting is almost always required to cover burnt area, which prevents secondary corneal complications.

Some advocate full-thickness burns with destruction of underlying muscle, bone and vital structures, separately as deep burns (Fourth-degree burns). Such burns require extensive and complex management and often result in severe contracture and prolonged disability.

Based on degrees and the likelihood of surgery, eyelid burns may be classified as:

• Minimal burns: Minimal burns are superficial partial-thickness burns that usually heal and do not require any surgery.
• Moderate burns: Moderate burns refer to deep partial-thickness burns that show delayed healing but may not require surgery.
• Major burns: Major burns are deep partial- or full-thickness burns and invariably require early surgery with skin grafting.

Exposure keratitis with or without secondary infection leads to conjunctival and corneal damage producing corneal opacities and, in severe cases, there may be destruction of globe.

Ocular surface examination:

Eyes should be examined under slit lamp (bio-microscopy) by an eye specialist.

Examination of eyes should be done as early as possible since eyelid usually swells and shut the eyes. Most ocular thermal injuries result in superficial burns to the cornea or conjunctiva.

Conjunctiva: Conjunctival oedema, if present, may be due to conjunctival surface burn, mild exposure, or due to fluid resuscitation. Look for any loss of conjunctiva due to burns. Involvement of both palpebral and bulbar conjunctiva may lead to formation of symblepharon (adhesion between palpebral and bulbar conjunctiva).

Cornea: Cornea may be examined under slit lamp after instilling fluorescein dye. Corneal injury is usually secondary to exposure, drying, and infection due to deep eyelid burns.

Initial assessment should note corneal sensation in order to appraise the risk of corneal ulceration from corneal exposure. There may be corneal thinning due to lagophthalmos.

• Superficial injury produces a spectrum of damage to epithelium ranging from minor punctate changes, to widespread loss of epithelium.
• In severe thermal burns, there is corneal opacification associated with extensive and deep damage to the tissues and it may result in stromal scarring. The resultant eschar eventually sloughs off, leaving a thin corneal tissue which is susceptible to corneal ectasia. Direct thermal damage to the cornea produces collagen shrinkage, with prominent stress lines. Collagen damage may lead to a rapidly excavating corneal ulcer originating from liquefactive necrosis. Globe rupture is seen in extreme cases.

Intraocular pressure monitoring and direct ophthalmoscopy is also required.

Extent of tissue damage is a prognostic indicator of recovery following ocular surface injury. Extent of damage to corneal, limbal, conjunctival tissues and intraocular structures influences the visual outcome and may be classified as:

Classification of ocular surface burns:

Dua (2001) provides a classification of ocular surface burns giving prognosis based on corneal appearance, conjunctival involvement and analogue scale recording the amount of limbal involvement in clock hours of affected limbus/ percentage of conjunctival involvement. The conjunctival involvement should be calculated only for the bulbar conjunctiva, up to and including the conjunctival fornices.

• Grade I: In Grade I, there is 0 clock hours of limbal involvement, 0% of conjunctival involvement, analogue scale reading of 0/0%, and the prognosis is very good.
• Grade II: In Grade II, there is less than 3 clock hours of limbal involvement, less than 30% of conjunctival involvement, analogue scale reading of 0.1- 3/ 1- 29.9%, and the prognosis is good.
• Grade III: In Grade III, there is between 3- 6 clock hours of limbal involvement, 30- 50% of conjunctival involvement, analogue scale reading of 3.1- 6/ 31- 50%, and the prognosis is good.
• Grade IV: In Grade IV, there is between 6- 9 clock hours of limbal involvement, 50- 75% of conjunctival involvement, analogue scale reading of 6.1- 9/ 51- 75%, and the prognosis is good to guarded.
• Grade V: In Grade V, there is between 9- 12 clock hours of limbal involvement, 75- 100% of conjunctival involvement, analogue scale reading of 9.1- 11.9/ 75- 100%, and the prognosis is guarded to poor.
• Grade VI: In Grade VI, there is total limbal (12 clock hours) involvement, total conjunctival (100%) involvement, analogue scale reading of 12/ 100%, and the prognosis is very poor.

Hughes (1946) classification (modified by Ballen in 1963, Roper- Hall in 1965 and Pfister et al in 1982) provides a prognostic guideline based on corneal appearance and extent of limbal ischaemia. The Roper-hall classification system was introduced in the mid-1960s and is the most established and commonly applied system.

• Grade I injury: In Grade I injury, there is corneal epithelial damage, no corneal opacity, no limbal ischaemia, and the prognosis is good.
• Grade II injury: In Grade II injury, the cornea is hazy but the iris details are visible. There is also ishaemia involving less than one third of the limbus and the prognosis is good.
• Grade III injury: In Grade III injury, there is total epithelial loss, stromal haze with obscuration of iris details, ischaemia of one third to one half of the limbus, and the prognosis is guarded.
• Grade IV injury: In Grade IV injury, the cornea is opaque with no view of the iris or pupil, the ischaemia is greater than one half of the limbus, and the prognosis is poor.

Differential diagnosis:

• Chemical injuries to the eyes.
• Ultraviolet radiation keratitis.
• Other causes of corneal opacification.
• Ocular cicatricial pemphigoid.]

Management should be carried out under medical supervision.

Thermal injuries can be devastating from both functional and psychological aspect to the patient. Complications of injuries may be minimised with prompt and adequate treatment. Barring severe and worst injuries, globe and good vision may be saved in most of the cases. Management is directed towards preserving the eye and vision, maintaining function, and restoration of cosmesis.

Any co-existing systemic inhalational burn injury should be treated.

Management of eyelids:

Medical therapy:

Immediate management of thermal injuries requires:

• Removal of any dirt and debris.
• Gentle removal of sloughed skin.
• Cold, moist compresses.

Subsequent management:

• Trimming of eyelashes: Singed eyelashes in thermal eyelid burn should be trimmed to avoid the possibility of char falling in the eye causing ocular surface discomfort. Blades of scissors may be covered with an eye ointment in order to prevent cut eyelashes from falling in the eye.
• Management of wound:

For mild first degree burns, cold compresses may be required in cases with significant eyelid swelling and drooping. Eyelid burns with no eyelid contraction may be treated conservatively with an antibiotic ointment.

Second- and third-degree burns with significant retraction causing lagophthalmos may require moist chamber or cellophane occlusion. If surrounding skin is severely burnt, surgical suture tarsorrhaphy may be done. Suture tarsorrhaphy is a temporary measure and may not prevent eyelid retraction. Suture tarsorrhaphy is not a substitute for eyelid repair with skin grafting.

Severe third-degree burns of the eyelids may require surgical relaxing incision over the burn eschar to release the cicatrising ectropion.

Surgical therapy:

• Temporary suture tarsorrhaphy: Temporary suture tarsorrhaphy is useful and effective in the presence of lagophthalmos caused by severe burn of the eyelid skin.
• Surgical tarsorrhaphy: Surgical tarsorrhaphy may be done at about two weeks when eyelid contracture usually occurs. It does not appear to prevent wound contraction where cicatricial ectropion is present. A combined lateral tarsorrhaphy with a skin graft produces good results. Since the risk of ectropion persists for months due to persistent eyelid shrinkage, a tarsorrhaphy should remain in place till the facial scar matures.
• Masquerade procedure: Masquerade procedure may be done to close the eye until further reconstruction, in severely damaged eyelids where no viable adjacent skin or tissue exists. All necrotic tissue including orbicularis oculi muscle and eyelid margins are excised and a conjunctival flap from the remaining upper and lower eyelid tarsal or bulbar conjunctiva is mobilised and sutured together. A split thickness skin graft is then applied to cover the entire eyelid area.
• Split-thickness dermal graft: Split-thickness dermal graft is an alternative in the presence of large corneal and scleral defects which cannot be covered by conjunctival flaps. The graft may be harvested from the thigh.
• Eyelid graft: Eyelid graft when applied in acute stage needs to be repeated several times, as a split skin graft contracts as compared to full thickness graft. If a thick skin graft is applied when all reaction to burns has subsided, one stage grafting suffices as the effect of contracting scars of adjacent tissues is minimised.

If both upper and lower eyelid requires grafting, to maximise the stretched graft bed for each eyelid, grafting is performed at separate times. The lower eyelid is operated first followed by upper eyelid.

Management of complications and sequelae of eyelids: The eyelids are evaluated at a later stage for retraction, tear pump function and cosmetic appearance.

• Trichiasis: Repeated electrolysis or epilation of trichiatic cilia may be required.
• Lagophthalmos: Lagophthalmos may be corrected by lower eyelid sling procedure.
• Medial or lateral canthus deformities: Multiple Z plasties or local transposition flaps may be required.
• Eyelid defects:

- Eyelid defect involving up to 1/3rd of the eyelid may be closed directly.

- Defects involving 1/3rd to 1/2 of the eyelid may be corrected by Tenzel s semicircular rotation flap.

- Defects involving more than 1/2 of the lower eyelid may be corrected by modified Hughes procedure (tarsal-conjunctival flap).

- Defects involving more than 1/2 of the upper eyelid may be corrected by sliding tarsal-conjunctival flap (variation of modified Hughes procedure).

- Defects involving entire lower eyelid may be reconstructed by Mustard cheek rotation flap.

- Large central defects of the upper eyelid may require Cutler- Beard procedure involving full thickness segment of the lower eyelid.

• Palpebral aperture stenosis: Cicatricial eyelid margins in full thickness eyelid burns causing palpebral aperture stenosis may require incisional release to relieve it.
• Canalicular obstruction: Burns around medial canthus may involve punctum and canaliculus. Daily puntal probing, punctoplasty and canaliculoplasty are the options.
• Eyebrow deformities: Depending upon the depth of the burn, eyebrow deformities may require a full thickness composite graft of hair bearing skin from temporo-parietal region.
• Scar revision: Scar revision with laser or surgical means may be required.

Management of ocular surface:

Preparation for vision restoration: Preparation for vision restoration must begin immediately after the injury. Deliberate and timely treatment determines successful outcomes in the rehabilitative process.

In succession, management consists of emergency treatment, pressure control, suppression of inflammation, enhancing stromal repair, and establishing eyelid-globe congruity during the early days, weeks, and months after the injury.

Topical or oral carbonic anhydrase inhibitors and topical beta blockers continue to form the mainstay of intraocular pressure control. Fibroblast inhibiting mitomycin C may improve the success of filtration surgery for glaucoma. Drainage procedures may be done if one or more filtration surgeries fail.

Operative procedures for ocular surface include amniotic membrane transplant, corneal epithelial stem cell transplants, keratoplasty, large-diameter lamellar keratoplasty, and keratoprosthesis.

Medical therapy:

Emergency management:

• Irrigation of eyes: Emergency management requires prompt irrigation and the removal of residual debris from the eye. Irrigation cools the ocular surface and removes any inflammatory substance. Any available neutral irrigation solution may be used in emergency. Solutions available for irrigation include normal saline, normal saline with bicarbonate, Ringer s lactate, balanced salt solution (BSS), and BSS- plus. No therapeutic differences have been noted among these solutions. After copious irrigation, necrotic corneal epithelium should be d brided to promote re-epithelialisation. Where possible, topical anaesthetic drops should be instilled to reduce pain and blepharospasm, thereby facilitating irrigation.

Acute and reparative phases:

After irrigation, better outcomes may be expected with prompt re-epithelialisation, while delayed or absent re-epithelialisation may require surgical intervention.

• Topical artificial tears: Topical artificial tears may be used as lubricant to the ocular surface to counter the effects of lagophthalmos.
• Topical antibiotics: Topical antibiotics may be used for any epithelial defects to prevent any secondary infection. Pseudomonas aeruginosa is the most common gram-negative organism which may infect the affected cornea.

Surgical therapy:

Surgical intervention that may help stabilising the ocular surface in severe thermal injury includes:

• Tenonplasty: Tenonplasty attempts to re-establish limbal vascularity in severe injuries and to promote re- epithelialisation. In this, all necrotic conjunctival and episcleral tissues are excised. Tenon s capsule is dissected with blunt instrument, and the resultant flap with its preserved blood supply is advanced to the limbus.
• Tissue adhesives (tissue glue): Tissue adhesives preserve integrity in the event of corneal thinning with impending or actual perforation of the globe. This is usually accompanied by the application of a soft bandage contact lens, which prevents glue dislodgement. Tissue glue can stop further melting by excluding inflammatory cells and their mediators. Tissue adhesives also provide a means of delaying penetrating keratoplasty.
• Amniotic membrane transplantation: Amniotic membrane transplantation may be used as supplement to surgical procedures where coverage of raw surfaces or suppression of inflammation is required. Amniotic membrane has anti-angiogenic (inhibitors of blood vessels growth) and anti-inflammatory proteins capable of suppressing the inflammatory response. Amniotic membrane can create a new basement membrane and promote epithelial healing. Amniotic membrane might be applied after a thermal injury following emergency services, usually weeks later. Despite benefits, amniotic membrane cannot replace the need for corneal stem cells.
• Corneal stem cell transplantation: Replacement of the corneal stem cells lost due to injury is important in restoration of an intact and normal corneal epithelial cell layer. These primitive, slow-cycling stem cells are located in the limbal area.

Monocular injuries allow for procurement of stem cells from the uninjured eye. When the injury is bilateral, Pfister (1993) showed that allografted limbal tissue was capable of restoring the stem cell population from an unrelated donor. Allografted corneal stem cells must be protected from the recipient immune process by systemic immune-suppression e.g. with cyclosporine.

• Corneal transplantation (Keratoplasty):

Success in restorative corneal surgery is governed by:

- Lid-globe congruity with normal blinking and the absence of corneal exposure. Preparatory procedures to lyse symblepharon, expand cul-de-sacs, and to eliminate lagophthalmos are often required to re-establish normal lid functioning.

- Quality and quantity of tear film.

- The presence of epithelial stem cells phenotypic for cornea.

- The absence of any current ulceration, inflammation, and/or uncontrolled glaucoma. Secondary glaucoma must also be controlled with medications or filtration surgery.

- Flawless surgical technique.

- Fresh corneal transplant tissue.

The value of preoperative use of LASER for blood vessels at the limbus in high-risk patients is controversial, but at least it reduces bleeding at the time of surgery.

If corneal surgery is delayed 18 months to 2 years after a burn, it increases the chances of success, especially in the absence of pre-existing ulceration, perforation, or glaucoma.

Penetrating keratoplasty: Penetrating keratoplasty refers to the full- thickness replacement of the affected cornea with a healthy donor. Penetrating keratoplasty may be used to provide tectonic support (such as in corneal thinning and perforation), and to improve visual outcome (such as in the replacement of corneal scarring).

Large-diameter penetrating keratoplasty: Replacement of the entire cornea and adjacent stem cells by large-diameter penetrating keratoplasty may be performed. One potential danger might be that such large transplants might interfere with the trabecular outflow channels and hence increase the likelihood of glaucoma. Proximity to the limbal blood vessels makes an immune rejection more likely.

Large-diameter lamellar keratoplasty: A very promising technique in corneal transplantation for injuries includes the use of 12 or 13 mm lamellar corneal transplants, along with the limbal epithelial stem cell population. Smaller lamellar transplants are useful to fill in deep corneal ulcerations, descemetoceles, or frank corneal perforations.

• Keratoprosthesis (Artificial cornea): In the most severe cases, implantation of a keratoprosthesis (e.g. Boston keratoprosthesis) might afford the only means by which vision can be restored.

Indications for keratoprosthesis are:

- Corneas exhibiting exuberant vascularity.

- Repeated failures of fresh transplanted corneal tissue.

- Chronic limbal stem cell deficiency.

- Inability to restore normal lid anatomy.

The operation is usually advised in patients with severe bilateral injuries where serviceable vision is not present in either eye. A surprising degree of success may be achieved with keratoprosthesis. Critical to the visual outcome of a keratoprosthesis is the control of intraocular pressure at all times after the injury. Complications of keratoprosthesis include corneal melt, infection, glaucoma and formation of retro-prosthetic membrane.

• Conjunctival transplantation: Conjunctival transplantation is a means of restoring conjunctival fornices following fibrosis. This provides compatible tissue with a basement membrane, unlike other mucosal replacements. The procedure involves taking a sample of upper bulbar conjunctiva from the contra-lateral (other uninvolved) eye.
• Buccal and Nasal mucosa transplant: Buccal mucosa grafts may be used to treat symblepharon (adhesion between bulbar and palpebral conjunctiva), trichiasis (misdirected eyelashes), distichiasis (partial or complete second row of eyelashes), or entropion. The graft is usually obtained from the posterior aspect of the upper or lower lip. The advantage of nasal mucosal grafts lies in the ability to obtain large sized grafts.

Prognosis:

The prognosis for severe injury is typically poor and may result in widespread damage to the ocular surface epithelium, cornea and anterior segment. However, in recent years, the prognosis of severe ocular burns has improved, with advances in the understanding of the physiology of the cornea and the resultant development of enhanced medical and surgical treatments. The final visual prognosis is influenced by:

• The extent of ocular damage.
• The timing and efficacy of treatment.]

Education and training regarding prevention of exposures in the workplace can help in preventing thermal injuries to the eye.

For general prevention, safety glasses may be used to safeguard eyes. Even these measures may not suffice in high-velocity (explosive) injury.