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Both immediate and delayed presentations exist for eye problems in burned patients. Accordingly, in burns, the structure and function of a normal eye can be disrupted by concurrent blunt or penetrating injury, electrical current, thermal energy, or chemical agents. After the initial insult, foreign bodies, ongoing chemical injury, deterioration of the facial burn wound, infection, and environmental exposure can cause additional damage or progression of existing pathology. Although many providers may view comprehensive eye examination as an esoterica outside their skillset and purview, the frequency and acuity of sight-threatening complications necessitate the burn team learning the basics of eye evaluation.
The organ of sight arises through reciprocal interaction between the optic vesicle (neuroectoderm) and the lens placode (facial ectoderm). The full-thickness neuroectoderm protrudes toward the surface, inducing the primordial lens, and invaginating to form the optic cup. The lens vesicle, separating from the surface ectoderm, induces corneal development. The upper and lower eyelids develop from primordial eyelid folds, fusing transversely from 8 weeks to 5 months, protecting the nascent ocular surface from initial environmental exposure as the fetal urinary system begins to contribute to the amniotic fluid composition.
Eyelids are four-layered structures of skin, orbicularis muscle, tarsus with fibrous septae, and palpebral conjunctiva. The skin of the eyelids is thin and elastic in the normal state. Upper eyelid skin folds are formed from terminal skin attachments of underlying levator muscle, which functions with Müller's muscle to open the upper eyelid. The inferior rectus muscle provides analogous function via the capsulopalpebral fascia and inferior tarsus, retracting the lower lid with down-gaze. The orbicularis muscle can be divided into pretarsal, preseptal, and orbital segments based on the structure they overlay: tarsus, orbital septum, or orbital rim. The pretarsal and preseptal parts are used in blinking and voluntary winking, while the orbital segments are used in forced closure. Motor innervation is via the zygomatic and temporal branches of the facial nerve. Epidermal appendages, including follicular sebaceous glands (of Zeiss), modified apocrine sweat glands (of Moll), and eyelashes, are located at the anterior margin of the mucocutaneous junction. Posteriorly, the fibrous tarsi harbor the Meibomian glands (about 50 in the upper lid and 25 in the lower lid) that secrete lipid-rich material into the tear film.
The tear film is a trilaminar structure; moving from the ocular surface externally, there is mucus on the cornea and conjunctiva, covered by an aqueous layer, with a lipid layer most externally. A healthy tear film remains stable for at least 10 s and maintains more than 300 µm of meniscus height. The lacrimal gland, located laterally and superiorly in the orbit, produces the aqueous phase of the tear film, along with accessory lacrimal glands (of Krause and Wolfring) located in the superior and inferior fornices. The lipid layer is secreted by the Meibomian glands, stabilizing the tear film and reducing evaporative loss. A complex protein mixture within the tear film confers antimicrobial, inflammatory, and antiinflammatory properties and regulates corneal epithelial cell function.
The conjunctiva covers the inner surface of the eyelids and the anterior sclera, reflecting between the two at the superior and inferior fornices. It is composed of stratified nonkeratinized squamous and columnar cells interspersed with goblet cells upon a continuous basement membrane and lamina propria. Other tissues include accessory lacrimal glands and immune surveillance cells; the lymphatic drainage of the conjunctiva is via the submandibular, parotid, and preauricular nodes. The limbus is the border between the conjunctiva and corneal epithelium. Circumscribing the limbus, the palisades of Vogt harbor the corneal epithelial stem cell niche.
The corneal epithelium is approximately 6–7 cell layers (50 µm) tall and composed of stratified squamous epithelium with minimal keratinization. The basal layer is mitotically active and replenishes the more external layers as they are continuously sloughed. The corneal epithelial stem cell niche, at the limbus within the palisades of Vogt, allows reepithelialization when the entire basal layer is lost, as in severe burn injuries or toxic epidermal necrolysis. This mechanism requires cell proliferation and migration from the limbus to the center of the cornea and can take weeks to fully reepithelialize the cornea, compared with days when the basal corneal epithelial layer remains intact. The corneal epithelium produces and rests upon a basement membrane. The layers deep to this basement membrane comprise the corneal stroma. The first 8–12 µm of stroma is called Bowman's membrane and is composed of randomly oriented collagen fibers. The stroma is approximately 500 µm (0.5 mm) thick. Precise arrangement of about 200 collagenous lamellae confers transmittance of visible light. Fibroblasts and immune surveillance cells populate the stroma. A deep layer, Descemet's membrane, about 10 µm in thickness, provides posterior structural integrity. Upon this membrane rests the corneal endothelium, rich in mitochondria and nonproliferative, which maintains corneal dehydration (and transparency) via active transport of solute into the aqueous. The cornea provides about two-thirds of the refractive power of a normal eye, approximately +40 diopters.
Eye examination in a burn ICU requires several modifications from the standard clinic setting. Clinicians must adapt to the overall patient condition and support machinery, which may include multiple intravenous and enteral access lines, ventilator and dialysis support, bulky wound dressings, difficult patient positioning, and, frequently, severe comorbid injuries and burns of the face. This is not the “comfort zone” for the ophthalmologist, but the frequency and acuity of comorbid eye involvement necessitate adaptation and innovation. An assessment of visual function can be made with a near vision card, finger counting, or, at a minimum, light perception. Patients with endotracheal tubes can generate various responses, head nod or hand signal, to visual acuity testing under appropriate sedative/analgesic conditions. There are a variety of portable slit lamps that can be employed. Our preference is a handheld lens (20 diopter or equivalent) and penlight. With practice, the penlight may be axially directed through the lens or shone indirectly upon the ocular surface to section through the anterior segment, thereby providing fine detail of stromal and corneal epithelial problems. Loupes provide additive magnification when used with a handheld lens. Topical ocular surface anesthesia is usually employed.
If the injury was associated with an explosion, with flying debris or blunt/penetrating trauma to the eye and periorbita, an open globe injury may result. In this situation, examination must be performed without pressure on the globe until corneal or scleral perforation can be excluded. Pressure applied to an open globe could cause (further) herniation of intraocular contents and detract from potential recovery. If an open globe–suspect injury is identified, pupillary light response and visual acuity should be grossly documented (at least light perception/hand motion/finger counting), photographs obtained, and a shield placed over the eye sufficient to transmit any applied pressure to the osseous orbital rim rather than the orbital contents. Immediate ophthalmological consultation is indicated to evaluate a possible open globe.
Once an open globe injury is excluded, cotton swabs, Desmarres retractors, or an eyelid speculum are useful and often necessary due to facial burns and lid edema. “Swelling” is never an excuse to defer examination of the ocular surface because any delay in the recognition of significant injuries subjects a patient's visual recovery to avoidable jeopardy. Superficial foreign bodies can usually be removed by saline irrigation alone if identified quickly postburn. Fluorescein dye (strips or equivalent) should be available in the burn unit and used if there is any suspicion of corneal or conjunctival pathology. The ocular surface should be irrigated to remove any discharge or ointment. A normal healthy cornea should appear clear and “glassy” with a sharp light reflex. A hazy light reflex can usually be appreciated in early-stage keratopathies. We generally apply dye in a balanced salt solution to the lateral canthus/inferior fornix and then have the patient blink a few times. Next the eye is opened and examined for epithelial irregularities and negative staining. Excess dye is then rinsed away with balanced salt solution. A normal healthy cornea will be devoid of stain; dye retention signifies pathology. Areas of confluent, homogeneous stain signify epithelial defect ( Fig. 43.1C ). “Lacey” staining patterns usually signify epithelial keratopathy ( Fig. 43.1B ). Early-stage epithelial lesions of exposure and herpetic keratopathies are often difficult to appreciate without the assistance of dye. Adjustable-intensity pocket LED flashlights often have fairly cool light, which sufficiently highlights fluorescein; otherwise, a cobalt-blue filter or near-ultraviolet hand-held light can be used. Photographs of findings often allow more comprehensive review while minimizing patient discomfort.
Indirect ophthalmoscopy via adilated pupil is occasionally useful and indicated in the burn unit. In cases of nonaccidental trauma, distinctive retinal lesions may be observed and should be documented with fundus photography for potential medicolegal review. In the first 48–96 hours following carbon monoxide intoxication, cerebral swelling and herniation syndromes are frequently causes of death. Funduscopy may show papilledema, which can be graded in severity. In cases where persistently positive blood cultures raise clinical concern for hematogenous seeding, infectious microemboli can occasionally be visualized on thorough funduscopy. Similarly there is a spectrum of retinal findings with disseminated candidiasis, defined as Candida isolated from three or more sites (urine, sputum, wound, blood, or eye). Because choroidal blood flow is much higher than retinal blood flow, these hematogenous lesions more frequently occur within the choroid and are initially observed underlying the retinal layers as gray-white round lesions, rather than occlusive lesions within the retinal vessels proper. These lesions, termed chorioretinitis, enlarge as the infection progresses and may erupt into the vitreous. This distinction is important because the stage/level of involvement determines treatment choices (ranging from intravenous antimicrobial therapy, intravitreal antimicrobial instillation, to vitrectomy for significant vitreitis).
Thermal injuries to the eye concurrent with the burning event are, fortunately, rare. The typical presentation is decreased vision, eye pain/foreign body sensation, perilimbal hyperemia, and epithelial defect with fluorescein staining. If detected early, a corneal epithelial lesion, analogous to a blister, may be present and is usually translucent to opaque. Upon sloughing, an underlying epithelial defect of varying depth is apparent. In the setting of closed-space (house) fires, it is difficult to determine whether a corneal injury is thermal or (gaseous) chemical in nature, and copious irrigation is recommended. In addition to tissue destruction, eyelid burns compromise the skin barrier function and predispose to burn wound cellulitis and infection. Development of a preseptal inflammatory process (eyelid swelling, hyperemia, and pain) is frequent after eyelid burn injury, and microbiological cultures help in determining whether this process is sterile or infectious. If infected, it is termed preseptal cellulitis. When observed, it is crucially important to evaluate extraocular muscle mobility and function. If the orbital septum is compromised, an orbital cellulitis or abscess may develop, which is an eye-threatening emergency. Typical presentation of orbital cellulitis or abscess includes reduced extraocular movements and pain on extraocular muscle testing. Ophthalmological consultation, systemic antimicrobial therapy, and frequent reexamination are indicated. Surgical débridement may be needed for orbital abscess.
Chemical eye injuries are a true ophthalmological emergency. Frequent and copious eye irrigation is generally indicated. Solid chemical particles should be removed by irrigation as rapidly as possible with upper and lower lid eversion and examination. Alkali injuries may need prolonged irrigation, up to several hours. Wound pH can be litmus tested, preferably 2–5 minutes after cessation of irrigation as early false-normal results may occur. Insertion of an irrigation aid, such as Morgan lenses, can provide continuous irrigation for several hours; these can also be useful for continuous antibiotic delivery in cases of refractory bacterial keratitis.
Patients with Stevens–Johnson syndrome/toxic epidermal necrolysis (TEN) are treated in the burn unit, and eye involvement is seen in more than 60% of these cases. At worst, they present with complete corneal slough, membranous conjunctivitis, and lash auto-epilation ( Fig. 43.1C ). The natural history is scar formation at involved areas, symblepharon, forniceal shortening, corneal opacification/scarring, mucocutaneous junction loss/keratinization, entropion, and chronic, severe, dry-eye symptoms. Mounting evidence indicates that ocular surface recovery may be hastened, with improvement in vision, by prompt coverage of the ocular surface with amniotic membrane. Patients with these conditions should receive definitive treatment at burn units where amniotic membrane transplantation is available and applied immediately when ocular surface involvement is apparent.
As with the systemic response, there are a number of unique ocular aspects of electrical burn injury. Cataract formation following electrical injury has been recognized for more than a half a century. While 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 following 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 ( Fig. 43.1B ). 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 prior to sloughing of the diseased epithelium. While 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/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 ( Fig. 43.1A ). 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 ( Fig. 43.1C ). 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 from the periphery. 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.
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