As with the systemic response, there are a number of unique ocular aspects of electrical burn injury. Cataract formation after electrical injury has been recognized for more than a half a century. Although the mechanism is not fully understood, within the lens (and other ocular tissues) there is substantial intercellular electrical coupling. These reports note that electrical cataract tends to present within 12 months of the electrical burn event and that visual outcome after cataract extraction can be good in the absence of other eye pathology. Other findings, such as chorioretinal atrophy, are seen less frequently. ^, For both patient care and medicolegal reasons, electrical injury patients should be evaluated for cataract via dilated exam at admission, discharge, and 6 and 12 months postinjury.

Eyelid burns and singed eyelashes identify a group of patients at high risk for ocular surface problems, with likelihood ratios (LR+), if present, for the development of corneal ulceration of 12 and 6.9, respectively. Punctate epitheliopathy, or keratopathy, is usually the earliest stage of per se corneal injury, and, if present, it confers an LR+ for the development of corneal ulceration of 6.4. These subtle irregularities on the normally glassy corneal surface can be discerned with magnification and are accentuated by the application of fluorescein dye (see Fig. 37.1 B). The severity of epitheliopathy ranges from scattered, superficial submillimeter dots to a homogeneous area of abnormal epithelium, confluent keratopathy. The latter is essentially an epithelial defect before sloughing of the diseased epithelium. Although keratopathy may be caused by direct thermal or chemical injury of the eye, it is much more frequently observed with corneal exposure resulting from the contraction of eyelid burn wounds and scars. It generally develops around 1 week postburn, and careful observation of the sleeping patient demonstrates incomplete resting eyelid closure, with scleral or corneal show (see Fig. 37.1 A). Any patient with incomplete lid closure, best observed while asleep, should undergo detailed examination of the ocular surface. Bell’s phenomenon, up-gaze with lid closure, is absent in 25% of patients and does not reliably protect the ocular surface when present; however, an intact Bell’s phenomenon may somewhat mitigate the severity of exposure keratopathy.

An epithelial defect is present when an area of the cornea has lost epithelium (see Fig. 37.1 C). It is denoted by a subtle ridge where epithelium remains and by a solid area of fluorescein staining. This can be either full or partial thickness. Partial-thickness epithelial defects can heal rapidly from the remaining basal layers, whereas full-thickness injuries must heal by keratinocyte migration from the periphery. Other than observing time to healing/reepithelialization, it is somewhat difficult to otherwise discern the depth/thickness of a corneal epithelial defect. If the basement and Bowman’s membranes are disrupted, keratinocyte migration will be further delayed, and more aggressive eyelid closure techniques (discussed later) should be considered in the interim. Typically the epithelial defect seen from incomplete eyelid closure (exposure) is transverse, linear, and centered over the inferior third of the cornea. Careful daily examination of epithelial defects is required in burn patients, as is correction of underlying causes. If magnified examination reveals stromal opacification (i.e., any finding other than clear cornea at and around the epithelial defect), then a corneal ulcer is present and there is a high risk of vision loss. All indicated diagnostic and therapeutic maneuvers should be employed without delay.

We define a corneal ulcer as an epithelial defect with any associated stromal infiltrate (see Fig. 37.1 E). Corneal transparency, or lack thereof, is an important finding with histopathologic correlates. Transparency is lost when the stroma becomes hydrated. In burns, this is typically in response to injury or infection. This occurs when the keratinocyte basement membrane has been compromised, a process that can develop independent of phagocytic cells via production of active matrix metalloproteinase-9 (MMP-9) and then MMP-2 by corneal cells. The active forms of these enzymes have also been observed in the tear fluid from ocular burn and infectious ulceration patients. Altered capillary permeability and the evolving wound-healing response occur in a manner akin to skin wound healing. This includes phagocytic infiltration, tissue destruction and pathogen clearance, reepithelialization, and myofibroblast-mediated scar formation. The disorganized collagen formed as part of scar formation lacks the regular arrangement and spacing of a healthy, clear corneal stroma. As a result, it appears white or gray and reflects, rather than transmits, visible light, causing vision loss. Transparency can also be lost as a result of corneal endothelial dysfunction. Impaired function of the endothelial adenosine triphosphate (ATP)-dependent transport of solute from the stroma into the aqueous humor causes abnormally increased hydration of stromal proteins. The associated epithelial defect should be measured daily at a minimum on magnified exam because stability (nonenlargement of the defect) followed by reepithelialization (decreasing size of the remaining defect) indicate treatment response. Inhibition of serine proteases may slow epithelial migration, although inhibition of MMPs may actually facilitate reepithelialization. A key point is that the majority of corneal ulcers can be prevented in burned patients via early release and skin grafting of deep partial- and full-thickness eyelid burns. The majority of corneal ulcers in burned patients are sterile, but bacterial superinfection is not uncommon. For this reason, and because treatment of infectious corneal ulcers is aided by the provision of directed antibiotics, swab or scraping culture of corneal ulcers is a routine part of our diagnostic protocol. Corneal scraping is accomplished with ophthalmic tetracaine drops, sedation (usually intravenous ketamine), loupe magnification, adequate lighting, and either a #69 or the rounded belly of a #15 blade. Carefully, the margin of the corneal ulcer is scraped, maintaining the edge of the blade almost parallel to the corneal surface to avoid any penetrating injury. The specimen, often visible only with loupes, is plated on blood and chocolate agars (for the broadest spectrum of bacterial growth), Sabouraud’s agar (for fungal organisms), and several glass slides, for Gram stain (for bacteria), Giemsa stain (for cellular features and viral cytopathic effect), and potassium hydroxide stain (for fungal elements). Rapid review of the slide specimens, if positive, enables immediate initiation of directed topical antimicrobial agents. Initial response to treatment is nonprogression (stabilization) in the size of the epithelial defect and underlying stromal infiltrate. With continued healing, these gradually become smaller. Therefore every follow-up examination should scrupulously document (and/or photograph) the sizes of the epithelial defect and stromal infiltrate.

Bacterial corneal ulcers can occur in otherwise healthy patients, as with prolonged use of contact lenses, but burned patients are at particular risk because of lost eyelid function, ocular surface exposure, local contamination from colonized/infected skin wounds, and disruption of host immunity, among other factors. Acinetobacter spp. have been reported, as well as Staphylococcus spp. and Pseudomonas spp. ^, Pathogen virulence factors play important roles in the outcome of these infections, and more virulent bacteria may be selected during the recovery of severely burned patients. Bacterial keratitis typically follows a more fulminant course than sterile corneal ulcers caused by exposure (see Fig. 37.1 F).

Burn patients are at risk for developing secondary infections of persistent exposure-related epithelial lesions. Not infrequently, fungal organisms are isolated as colonizers or active pathogens from burn wounds of the face and eyelids; thus facial wound microbiology determines the risk of secondary infection at ocular surface lesions. We have seen secondary Candida keratitis (ulcer) arising in this manner. Fungal keratitis is typically more indolent and is unresponsive to antibacterial treatment. With magnification, satellite lesions may be observed around the primary lesion. Diagnosis can be made through scraping, potassium hydroxide prep, and fungal culture. A corneal biopsy is rarely necessary to establish the diagnosis if a high clinical suspicion for fungal keratitis exists while cultures remain negative. In refractory cases, debridement and corneal transplant may be necessary.

The systemic response to burn injury entails profound alterations in host immunity, including markedly reduced novel immunoglobin generation and adaptive cell-mediated immunity. Type 1 T-helper (T _H 1) cellular response, activated macrophage cell killing, is associated with clearance of systemic virus and survival in animal models. Elegant studies by Suzuki et al . demonstrated that, postburn, chemokine CCL2 (a.k.a. monocyte chemoattractant protein-1) stimulates a subset of natural killer T cells to produce interleukin-4, an early signal in a cascade ultimately producing T _H 2 cytokines and abolishing the beneficial T _H 1 response. This situation leads to increased susceptibility to Herpesviridae. Herpetic keratitis (reactivation) in burned patients is both a sight-threatening problem and a marker of profoundly altered immunity. Dendritic (branching) epithelial defects and stromal infiltrates are typical of herpetic keratopathy (see Fig. 37.1 D). Allowed to progress, these enlarge forming a “geographic” corneal ulcer with an irregular border. Real-time polymerase chain reaction testing of corneal swab specimens is invaluable for diagnosis, providing rapid (within hours) information about the presence and type of Herpesviridae infection. Although tear specimens have also been studied, the diagnostic yield is substantially lower.

Orbital compartment syndrome (OCS) occurs when the globe is compressed by swelling of the orbital contents and is unable to decompress itself. The natural variation in eyelid laxity provides a variable individual susceptibility to this problem; if the globe is able to move anteriorly to accommodate the swelling, intraocular hypertension may not develop. Acute intraocular hypertension can lead to anterior ischemic optic neuropathy (AION), with loss of vision. In the setting of severe burns, it can rapidly cause complete loss of vision bilaterally. Decreased arterial pressure further compounds the risk of AION infarction. Orbital compartment syndromes are occasionally observed in the first 24 to 96 hours after severe burn injury requiring large-volume resuscitation. The development of compartment syndromes in unburned extremities or abdomen should prompt evaluation of the intraocular pressure; urgency is increased if there is concomitant arterial hypotension. Burns of the face and periorbita can lead to prodigious swelling and OCS in the absence of massive fluid resuscitation. Full-thickness flame burns (charring) and eschar of the periorbital skin can prevent the normal swelling of the underlying tissues, thus facilitating OCS. Intraocular pressure can be evaluated grossly by direct palpation of the globe, by evaluating the mobility of the globe against the lower lid (the globe is tightly pressed against the conjunctival surface of the lower lid in OCS), or more exactly with a Tono-Pen or Schioetz tonometer. Intraocular pressure is sensitive to extrinsic forces, so it is essential that the technique used to open the lids not compress the globe or a falsely elevated intraocular pressure reading may result. Measured at the cornea, intraocular pressures of 20 mm Hg or higher are cause for concern and frequent reevaluation. Avoiding excessive fluid/volume expansion and elevation of the head of the bed can help reduce intraocular pressure. If the globe is hard on palpation, the lower lid is tightly apposed to the globe, or intraocular pressure remains at 30 mm Hg or higher, release of OCS is indicated to preserve vision and prevent AION. The intraocular pressure threshold for release should be somewhat lower when patients have shock with ongoing arterial hypotension because tissue perfusion is a balance between arterial and tissue hydrostatic pressures.

Amblyopia is concerning in the burn unit primarily when prolonged eyelid closure or near-closure is requisite to treat ocular surface lesions in prepubertal children. Loss of visual stimuli leads to loss of capacity to perceive visual stimuli. Amblyopia presents with decreased visual acuity in the absence of structural or refractive lesions. In practice, it is better to treat both eyes equally (e.g., tarsorrhaphy) if eyelid destruction and ocular surface exposure are present. In cases where vision is unilaterally affected, it is possible to intermittently patch, or treat with cycloplegics, the “good” eye, in an attempt to prevent amblyopia. Involving an ophthalmology consultant is prudent when vision-preserving eyelid procedures raise concerns for iatrogenic amblyopia.

The posterior 50 μm of corneal stroma is Descemet’s membrane. This posterior layer of corneal stroma, although thin, possesses a high degree of strength. When stromal destruction is near full thickness, the aqueous humor of the anterior chamber may be contained by this structure alone. Termed a descemetocele , it is a sign of an impending corneal perforation (see Fig. 37.1 G). Often an aqueous leak can be appreciated if fluorescein dye is applied over the area; the leaking aqueous humor dilutes and carries the dye into the tear lake (positive Seidel test). Corneal perforations (see Fig. 37.1 H) and lacerations ( Fig. 37.2 ) can be similarly recognized if the aqueous leak is not massive. With a massive loss of aqueous humor, the eye loses intraocular pressure, becoming “flat.” Loss of intraocular pressure, or marked intraocular hypotension below 8 mm Hg, can result in choroidal detachment and loss of retinal function. Early application of tissue adhesive to descemetocele or acute perforation reduces the rate of eventual enucleation. ^,

(A) Corneal laceration; (B) Scleral laceration.

Lenses useful as corneal bandages are characterized by low diopteric power, soft structure, and high gas permeability, and are often labeled extended wear (e.g., Bausch and Lomb Night and Day or Acuvue Oasis). These are occasionally useful in facilitating reepithelialization and protecting corneas damaged by exposure. Once in place, these lenses should be evaluated frequently and discontinued or replaced when no longer effective. Because of risk of infection and other complications, it is prudent to involve an ophthalmology consultant when bandage contact lenses are employed.

Lateral canthotomy should be performed in cases of OCS, described earlier. Structure is provided to the lids by the canthal tendons, inserting on the upper and lower tarsi medially and laterally. The lateral origin is palpable as a bony prominence at the lateral orbital rim, called Whitnall’s tubercle. Lateral canthotomy is performed by dividing the skin and lateral canthal tendon, freeing the lower lid from its bony attachment. Lidocaine 1% or 2% with epinephrine is infiltrated lateral to the lateral canthus and the skin is clamped parallel to the palpebral fissure, then divided with scissors anteroposteriorly. The lower lid is grasped and pulled away from the globe, placing the lateral canthal tendon on stretch, making it easier to locate and divide. The canthal tendon is divided with scissors anteriorly to Whitnall’s tubercle on the orbital rim. ^, A successful lateral canthotomy leaves the lower lid freely mobile and no longer apposed to the globe. Afterward, the intraocular pressure should be reevaluated.

Because the vast majority of burn-related eye disease results from exposure of the ocular surface, techniques facilitating eyelid closure are of central import. Temporary closure can be accomplished with wound closure strips and cyanoacrylate skin adhesive; this closure may last 24 to 48 hours. Cyanoacrylate adhesive can also be used to temporarily close the lids by joining the lashes and eyelid margins of the lateral parts of lids; in practice, this method of temporary eyelid closure lasts a few days. A temporary suture tarsorrhaphy can be constructed either with bedside sedation and local anesthesia or in the operating room. Tarsorrhaphy increases the rate of corneal epithelial wound healing. ^, Several techniques have been described; some permit facile reopening and reclosure if frequent eye examination is deemed necessary. Chromic gut sutures often do not require removal and are occasionally used in our practice. A tarsorrhaphy becomes progressively more “permanent” as deepithelialized surfaces of the eyelids are apposed. Several methods exist to create what we term semipermanent tarsorrhaphy; these are indicated when large areas of full-thickness injury to the eyelids necessitate multiple reconstructive operations or after the failure of previous temporary suture tarsorrhaphy. Less durable outcomes are associated with mattress sutures or bolster techniques than an internal fixation technique by which the gray line is split in the region of the planned tarsorrhaphy and the posterior and anterior laminae of the upper and lower lids are sutured to each other. It is vitally important to avoid placing knots in contact with the corneal surface because these can cause abrasion injuries and corneal ulcers.

The forces of scar contraction powerfully influence eyelid function and, when tarsorrhaphy (including temporary) is indicated, often eyelid release and tissue interposition will also be required to preserve sight ( Fig. 37.3 ). Essentially the procedure is a reverse blepharoplasty: the skin and scar of the lid is incised in the tarsal crease, and the upper lid mobilized inferiorly. Overcorrection is needed at the time of surgery because recurrent contraction in 2 to 3 weeks is the rule. The resulting defect can be covered with a split-thickness skin graft and secured with a combination of fibrin glue, sutures, or cyanoacrylate adhesive. If necessary, a secondary procedure is employed for the lower lids, although full-thickness skin autografts may be substituted to close the defect after release. Although release and skin graft interposition may protect a fresh tarsorrhaphy from disruption caused by scar contraction at the eyelids, these grafts eventually contract despite all efforts at preservation. Contraction and recurrence of cicatricial ectropion necessitate a series of repeated releases until both ocular surface and eyelid function stabilize. In cases of massive burns, when eyelid release is required and no sufficient donor site for sheet grafting of the upper lids can be spared, it is possible, despite burned skin, to mobilize the midportion of the brow and upper lid inferiorly from the medial and lateral brow in a myocutaneous V-Y inferior advancement flap, akin to this flap’s utilization in oncologic reconstruction. This procedure may provide the release needed to allow formation of a stable tarsorrhaphy for ocular surface protection in critically injured patients.

(A) Upper eyelid release, grafting, and lateral tarsorrhaphy; (B) Follow-up.

Huang et al. suggest use of local skin flaps, when possible, to overcome the difficulty of autograft contraction and recurrent cicatricial ectropion. The lower lid may be treated with a superomedially based island pedicle flap from the nasolabial fold ( Fig. 37.4 ). This flap is quite durable, and the donor site heals with little morbidity. If burn scar of the skin surrounding the donor site precludes closure, a split-thickness autograft can be used. Flaps available for the upper lid include paramedian forehead flap and orbicularis oculi myocutaneous flap from the lower lid with a laterally based pedicle ( Fig. 37.5 ). ^, The lower lid donor site defect of the latter may be closed with the previously discussed nasolabial fold island pedicle flap. Occasionally, the tissue destruction resulting from burn injury is so severe that the structural integrity of the tarsal plate is compromised. This leads to lid dysfunction often recalcitrant to the preceding methods of treatment. To address this, tarsal compromise must first be recognized. It can be replaced using suitable cartilage, often harvested from the conchal bowl. Placed in a preseptal location during eyelid contracture release and covered with a skin flap, this technique can be used in cases of subtotal eyelid loss so long as intact palpebral conjunctiva remains. Replacing lost conjunctival tissue is infrequently necessary postburn. This deformity can present with entropion and significant ocular surface injury and is frequently seen after Stevens-Johnson syndrome or TEN. We have successfully employed the technique of preseptal cartilage graft with skin resection (blepharoplasty) to rotate the lash line and scarred/keratinized mucocutaneous junction away from the corneal surface. We have not yet had occasion to resort to conjunctival replacement procedures, such as buccal or nasal mucosal free grafts or nasal septal composite cartilage-mucosa grafts. ^,

Cicatricial ectropion of the lower lid; reconstruction with nasolabial island pedicle flap. (A) Flap dissection; (B) Flap inset; (C) Follow-up.

Cicatricial ectropion; reconstruction with myocutaneous orbicularis flap and nasolabial flap. (A) Flap dissection; (B) Flaps inset; (C) Follow-up.

When corneal ulceration and epithelial loss are catastrophic and refractory to the previously described therapeutic measures, it is possible to mobilize the bulbar conjunctiva over the cornea ( Fig. 37.6 ). These flaps provide a supply of vascularized tissue to create scar, deliver systemic antimicrobial therapy to the wound, and stabilize an impending perforation (e.g., descemetocele). A fornix flap is constructed by suture of the mobile conjunctiva in the inferior and superior fornices. This flap may last 1 to 2 weeks before retracting and does not require any dissection. If small strips of apposing conjunctiva are excised, a more durable fornix flap may be held in place by adhesions similar to those formed via semipermanent tarsorrhaphy. Khodadoust described a microsurgical conjunctival flap, but its placement is more demanding than other options. The classic Gundersen flap mobilizes the superior bulbar conjunctiva over the entire corneal surface, beginning through a transverse incision of the conjunctiva in the superior fornix. After the superior bulbar conjunctival flap is raised, a perilimbal peritomy is performed, the cornea deepithelialized, and the flap brought down over the cornea by securing its inferior edge between the 4 and 7 o’clock positions of the periotomy. ^, The superior aspect of the flap is sutured to Tenon’s capsule between the 10 and 2 o’clock positions of the peritomy, and the entire superior surface of the globe is left denuded of conjunctiva, which rapidly reepithelializes. This flap is useful if performed with scrupulous avoidance of “buttonholing,” as holes created in the flap invariably expand and allow corneal exposure. The goal of a Gundersen flap is to provide long-term corneal coverage, prevent perforation, and preserve an intact globe for later vision restoration.

Gundersen (conjunctival) flap.

Rarely, burn injury or resulting scarring compromises the normal flow of tears through the lacrimal system. Although a Jones tube or lacrimal stent may be useful in other settings, in the burned patient, scarring and markedly abnormal function of the eyelids combined with discharge caused by chronic conjunctivitis render these tubes prone to clogging. The foreign body may also trigger local infectious complications. Instead we employ a conjunctival mucosal flap to create a fistulous tract for tear drainage. In cases where the punctum and upper lacrimal drainage apparatus are destroyed, this flap can be placed within the lacrimal sac, termed mucosal conjunctivodacryocystostomy. When the upper and lower lacrimal drainage structures are dysfunctional, the mucosal flap can be drained directly into the nasal or maxillary sinus cavities, mucosal conjunctivorhinostomy, and mucosal conjunctivoantrostomy, respectively. Refractory epiphora has been amenable to these treatments in 16 of 17 reported cases.

A stable ocular surface is generally requisite to achieve a successful corneal transplant. ^, Eyelid malposition must be corrected and epithelial defects and corneal ulcers closed and in a stable, if scarred, state. Corneal neovascularization frequently follows the healing of corneal ulcers. If present, it will increase the risk of corneal allograft rejection, as does the presence of nonnative immune surveillance (Langerhans) cells. Herpetic keratopathy is a further risk factor for rejection. Thus a lamellar graft (partial-thickness corneal allograft) is preferred, because it preserves the patient’s native endothelium from graft rejection. Lamellar grafts are also more tolerant of elevated intraocular pressure, although they can undergo epithelial or stromal rejection. As a salvage procedure, tectonic grafts can be used in the setting of frank perforation or descemetocele. The purpose of these procedures is to maintain a closed globe and intraocular pressure. Amniotic membrane multilayer grafts may be useful as a temporizing measure and may play an antiinflammatory role in decreasing the rate of rejection of allografts placed in an emergent setting. Rarely, destruction of the eyelids, ocular surface, and/or ocular surface may lead to the situation in which the potential for vision exists, but no native reconstructive options exist. These cases may benefit from evaluation by centers experienced in the performance of and postoperative care for keratoprosthesis surgery.