Neoplasms • 13 SECTION

149CarcinomaHAPTERellC Squamous •

Neoplasms • 13 SECTION

PROPHYLAXIS

Prevention is ideal; all individuals should be encouraged to avoid sunshine exposure and to use protective clothing and sun-blocking agents (SPF 50). The use of preventive methods should be particularly emphasized to those patients who are diagnosed with precancerous or cancerous skin lesions, who have a genetic history of skin cancers, or who have both.

TREATMENT

Systemic

Systemic or intralesional chemotherapy, or both, has been effective when used in conjunction with surgery or radiation. Topical 5-fluorouracil (5-FU) has proved to be efficacious in the treatment of solar keratosis, but 5-FU should not be used for the treatment of squamous cell carcinoma. Topical 5-FU may mask deep extension of the carcinoma.

Surgical

Surgical excision is the treatment of choice. The modified Mohs’ fresh tissue technique provides the best chance of complete tumor resection by controlling the tumor margin with frozen sections. The modified Mohs’ technique is modified when a pathologist, who is not the surgeon, performs the histologic evaluation of the frozen section specimens. With a standard Mohs’ technique, the surgeon prepares and reads the specimens; the standard Mohs’ technique is best reserved for those with special training in dermatopathology. Specimens are sectioned in a plane parallel to the outer painted edge so that the entire periphery is microscopically examined. Margins positive for the tumor are depicted on a map of the resected area, and additional peripheral sections are obtained until all margins are negative for the tumor. If removal of the lesion is other than a full-thickness eyelid resection, the deep base of the tumor must be carefully examined for deep extension. More generous tumor-free margins should be excised than those excised with basal cell carcinoma. The success rate of this method relates directly to the meticulous care taken by both the surgeon and pathologist. Mohs reports a 5-year cure rate of 98% of eyelid squamous cell carcinomas in the 213 patients he has treated. In cases in which the tumor is extensive and penetrates into the orbit, the treatment of choice is orbital exenteration. In cases of metastasis to regional lymph nodes, radical neck dissection should be considered in conjunction with adjunctive radiation or chemotherapy.

Cryotherapy

This is effective treatment for precancerous lesions (actinic keratosis) and as adjunctive treatment after excision of malignant squamous cell carcinoma. The technique requires freezing the tumor and a 5mm to 6mm margin of surrounding ‘normal’ tissue, with a liquid nitrogen cryotherapy probe or spray, and

then allowing the tissue to thaw before refreezing. Complications include lacrimal obstruction, skin depigmentation, loss of eyelashes and development of eyelid deformities requiring surgical reconstruction.

Radiation

Squamous cell carcinoma is relatively radioresistant. Radiation is an inaccurate method of determining the extent of the tumor because treatment is based solely on the radiation oncologist’s clinical impression. Radiation is generally reserved for extensive tumors that are surgically inaccessible, usually after tumor debulking. Large radiation doses in the range of 20 to 60 Gy are required, so proper shielding of the eye is imperative. A control rate of 93.3% at 5 years has been reported with radiation therapy.

COMMENTS

Squamous cell carcinoma is a malignancy arising from differentiated cells in the epidermis and must be diagnosed early and managed correctly to ensure a favorable outcome. The majority of periocular squamous cell carcinomas arise from ultraviolet light damage secondary to sun exposure. Older, fair-skinned individuals with previous extensive sun exposure are particularly prone to developing squamous cell carcinoma. Tumors arising from solar damage tend to have a lower rate of metastasis.

The clinical presentation of squamous cell carcinoma may mimic that of other skin tumors, so a high index of suspicion is required to establish an early diagnosis. All suspicious lesions require a biopsy with histologic evaluation. Surgical excision with a modified Mohs’ fresh tissue technique followed by plastic reconstruction of the site provides the optimal opportunity for complete tumor elimination while maintaining acceptable function and cosmesis. Patients who have developed one skin carcinoma are at a greater risk of developing new carcinomas and recurrences and require periodic reevaluation for the remainder of their lives.

REFERENCES

Christenson LJ, Borrowman TA, Vachon CM, et al: Incidence of basal cell squamous cell carcinoma in a population younger than 40 years. JAMA 294:681–690, 2005.

Dryden RD, Engen TB: Squamous cell carcinoma. In: Fraunfelder FT, Roy FH, eds: Current ocular therapy. 5th edn. Philadelphia, WB Saunders, 2000.

Mohs FE: Micrographic surgery for the microscopically controlled excision of eyelid cancers. Arch Ophthalmol 104:901–909, 1986.

Reifler DM, Hornblass A: Squamous cell carcinoma of the eyelid. Surv Ophthalmol 30:349–365, 1986.

Wilkes TD, Fraunfelder FT: Principles of cryosurgery. Ophthalmic Surg 10:21–30, 1979.

150 ACID BURNS 940.9

James P. McCulley, MD, FACS, FRCOphth

Dallas, Texas

Dipak N. Parmar, BSc(Hons), MBBS, FRCOphth

Dallas, Texas

Acid injuries of the eyes are characterized by protein coagulation and precipitation with the anion, with direct tissue damage produced by the hydrogen ion. These injuries tend to be less severe than alkali burns because the tissue proteins of the epithelium and superficial stroma serve as a buffer for the action of the acid, localizing its damage to the anterior cornea. In addition, most exposure to acids involves mild or moderate strength solutions. The prognosis for complete corneal epithelial healing is good in such cases, provided there is only limited damage to limbal stem cells. However, very strong acids penetrate the stroma just as quickly as alkalis, leading to a far worse prognosis with corneal opacification, anterior chamber pH alteration, and anterior segment destruction.

TREATMENT

Immediate

●Immediate copious irrigation of the eyes is of paramount importance, using either normal saline or water for at least 20 to 30 minutes. Both solutions are widely available, but their low osmolarity relative to the cornea leads to influx of fluid into the stroma, with possible diffusion of the corrosive into deeper corneal layers. Balanced saline solution is a better irrigation fluid in this regard, with an osmolarity equal to aqueous humor and enhanced buffering capacity (isotonic citrate and sodium acetate) that prevents corneal swelling and preserves the corneal endothelium.

●If possible, measure the pH of the inferior cul-de-sac prior to irrigation.

●After initial irrigation, allow 5 minutes for equilibration, then measure cul-de-sac pH. If the pH remains abnormally low, continue irrigation and check.

●Debride any necrotic corneal epithelium to allow normal tissue to re-epithelialize.

●Evert the upper lid to remove any trapped particles that can be associated with the acid.

ETIOLOGY

Sulfuric acid, a widely used industrial chemical and acid for batteries, is the most common cause of acid injury. Hydrofluoric acid causes the most serious acid injuries because of the small size of the acid molecule and its low molecular weight, which allows easy tissue penetration of the toxic fluoride molecule. Other frequently encountered causes of acid injury include sulfurous, hydrochloric, chromic, acetic, and nitric acids (Figure 150.1).

COURSE/PROGNOSIS

Acute phase (0 to 3 days)

●Injection, chemosis, ‘ground glass’ corneal epithelium, corneal epithelial defects, limbal blanching, corneal clouding.

●Severe pain, photophobia, decreased visual acuity.

Intermediate phase (3 to 7 days)

●Anterior uveitis.

●Severe burns: corneal ulceration, perforation.

Chronic phase (severe burns)

●Corneal vascularization, symblepharon formation, limbal stem cell deficiency, scarring and pseudopterygia (Figure 150.2).

●Anterior segment damage: iris atrophy, cataract, glaucoma.

Medical

●Antibiotic prophylaxis for bacterial infection, preferably with a broad-spectrum agent such as a fluoroquinolone, is necessary until corneal epithelialization is complete.

●Topical steroids decrease inflammation and reduce damage caused by proteolytic enzymes released by inflammatory cells. Prednisolone 1% or dexamethasone 0.1% eyedrops should be applied intensively for 10 days if the epithelium is not healed or for as long as the inflammatory process dictates, if the epithelium is intact.

●Cycloplegic agents, such as scopolamine, can be administered several times daily to reduce painful ciliary spasm and prevent posterior synechiae formation in the presence of anterior uveitis.

●A large therapeutic soft contact lens promotes re-epitheliali- zation of the cornea under the lens.

●Lubrication with preservative-free tears and lubricating ointment is required, as there is usually damage to conjunctival goblet cells and accessory lacrimal glands, in addition to sensory nerve damage impairing the corneo-lacrimal reflex arc. Autologous serum drops have been shown to promote epithelial healing in difficult cases, but topical antibiotic should be used to cover the additional risk of infection.

●Collagenase inhibitors are indicated in cases with evidence of collagen breakdown (stromal melt), which usually appears at 7 to 14 days after injury. The only available topical agent

Injuries Nonmechanical and Mechanical • 14 SECTION

151 ALKALINE INJURY 940.9

F. Hampton Roy, MD, FACS

Little Rock, Arkansas

A splash of an alkaline solution into the eye causes an immediate rise in the pH that can result in the damage or death of the vital external ocular tissues (the corneal and conjunctival epithelium), the protective envelope (the cornea and sclera), and the intraocular tissues (the trabecular meshwork, iris, ciliary body, and lens). Alkali rapidly penetrates the cornea and sclera, causing saponification and lysis of cell membranes, denaturation of collagen, and hydrolysis of glycosaminoglycans. The severity of the injury is dependent on the anion concentration, the duration of exposure, and the pH of the solution. It is important to document exactly the degree of injury with respect to the extent of epithelial loss on the cornea and conjunctiva, as well as the corneal stromal opacity and perilimbal whitening. Accurate classification of the burn is the key to making the most probable prognosis.

ETIOLOGY/INCIDENCE

The most common cause of a severe alkali injury of the eye in the United States is an assault. Data gathered from a large urban hospital show that young black men are at greatest risk, usually in a domestic setting where there is low-income, highdensity housing and a record of alcoholism and prior assaults. In the industrial sector, approximately 10% of 52,142 cases of ocular trauma reported from 16 states were chemical burns (1.6% acid and 0.6% alkali). Safety monitors have reduced the incidence of job-related eye injuries, but despite such programs, the storage and use of powerful alkalis, under extreme pressure and high temperature, continue to pose serious threats even to the properly attired worker wearing protective clothing and goggles. Farmers using liquid ammonia (ammonia causes the most serious alkaline injury) as fertilizer and homeowners using powerful cleansing agents, usually without eye protection, continue to be at special risk. The most common alkaline injury agent is lime.

COURSE/PROGNOSIS

The pain, lacrimation, and blepharospasm following an ocular alkali injury result from direct stimulation of free nerve endings located in the epithelium of the cornea, conjunctiva, and eyelids. With severe burns of the cornea and sclera, there is a sudden, spiking rise in the intraocular pressure that lasts about 10 minutes and is caused primarily by shrinkage of the collagenous envelope of the eye. A more prolonged rise in pressure quickly follows, secondary to prostaglandin release. Strong alkali rapidly penetrates into the eye, and the hydroxyl ions might remain for up to 2 hours, overcoming the poor buffering capacity of anterior segment tissues and the aqueous humor. Within 1 minute, the severe rise in aqueous humor pH causes lysis of corneal cells as well as of those lining and adjacent to the anterior chamber, compromising the blood-aqueous barrier and releasing necrotic debris into the aqueous humor. This leads to a severe fibrinous inflammatory reaction in the entire anterior segment of the eye.

Glaucoma may ensue because of inflammatory products accumulating in the aqueous humor and chamber angle, which promotes anterior synechial closure, especially inferiorly. The trabeculum and ciliary body may be injured directly by penetration of alkali through the sclera or by contact with alkalotic aqueous humor percolating through the meshwork. Ocular hypertension, hypotension, or both may occur at different times, depending on the aqueous dynamics occurring at that particular time. Chemical injury to the iris, crystalline lens, or ciliary body may produce mydriasis, cataract, or phthisis bulbi, respectively. Externally, this inflammatory reaction may be so profound as to lead to extensive symblephara and even ankyloblepharon caused by the apposition of raw conjunctival surfaces.

DIAGNOSIS

It may take 48 to 72 hours after the injury to correctly assess the degree of ocular damage and to offer an accurate prognosis. Classification of the degree of corneal opacification and of perilimbal whitening quantifies the extent of the injury and best projects the likely outcome:

●If mild corneal epithelial erosion and faint anterior stromal haziness are present and there is no ischemic necrosis of perilimbal conjunctiva or sclera, healing with little or no corneal scarring will result, and the visual loss will usually be no greater than one to two lines.

●When moderate corneal opacity and little or no significant ischemic necrosis of perilimbal conjunctiva have occurred, the epithelium will slowly heal, with moderate scarring and peripheral corneal vascularization, and a visual loss of two to seven lines may occur.

●Moderate to severe damage causes sufficient corneal opacity to blur iris details, and whitening of perilimbal conjunctiva is limited to less than one third. Corneal healing will be prolonged, and significant corneal vascularization and scarring will take place. The prognosis for visual acuity is usually limited to 20/200 or less.

●The blurring of the pupillary outline, ischemia of one third to two thirds of the perilimbal conjunctiva, and often a marbleized cornea indicate severe damage. Very prolonged corneal healing with inflammation and a high incidence of corneal ulceration and perforation are common. In the best cases, severe corneal vascularization and scarring result in counting-finger vision.

●When the pupil is not visible, more than two thirds of the perilimbal conjunctiva is ischemic, and the cornea is completely marbleized, only a very poor prognosis can be made. Corneal healing may be prolonged and show very severe corneal vascularization and scarring. The most severe cases show relatively rapid conversion of stroma into a necrotic sequestrum, with corneal perforation occurring through a thoroughly degraded corneal stroma. Phthisis bulbi is not uncommon.

TREATMENT

Ocular

The eyes should immediately be irrigated with copious volumes of an innocuous aqueous solution available at the scene of the injury and on the way to the hospital. Ocular irrigation with lactated Ringer’s or other available intravenous solutions should

151 CHAPTERInjury Alkaline •

Injuries Nonmechanical and Mechanical • 14 SECTION

be continued in the emergency facility for at least 2 hours or until the pH of the cul-de-sac has returned to neutrality. The intravenous tubing may be hand-held or, alternatively, a scleral shell with an inflow tube (Mediflow lens) may provide a more efficient method of delivering fluid to the eye.

●The sticky paste of lime (calcium hydroxide) may be removed from the conjunctiva with cotton-tipped applicators soaked in 0.01 M edetate calcium disodium.

●Mydriasis and cycloplegia should be induced with a 1% atropine instillation twice a day.

●Antibiosis is effected by topical application of a broad spectrum of antibiotics four times per day as long as an epithelial defect persists.

●Analgesics and sedatives are often required during the first several days for patients who have sustained severe burns.

●Glaucoma occurring after the injury commonly responds to carbonic anhydrase inhibitors such as 125 mg acetazolamide PO q.i.d. or topical 0.5% timolol b.i.d.

●Extensive destruction of the palpebral conjunctiva or eyelid skin may cause lagophthalmos and consequently exposure keratitis, a condition poorly tolerated by the damaged cornea. In these cases, use of an ointment and coverage of the affected eye with plastic wrap or a plastic bubble provide an immediate moist chamber to protect the cornea.

●Patching is only occasionally helpful in less severe injuries, when the redevelopment of epithelial defects simulates recurrent corneal erosions.

●The persistence of corneal epithelial defects correlates with the incidence of sterile ulcerations and increases the likelihood of infection.

●Soft contact lenses may facilitate re-epithelialization by acting as bandages to protect fresh epithelium from exposure to the air and by reducing the shearing stress of blinking. Disposable or extended-wear soft contact lenses are preferred. The use of 0.5 normal saline drops hourly and lubricants four times daily helps to maintain adequate hydration and lens mobility.

●If the epithelium can be encouraged to re-cover the cornea, stromal healing is accelerated and the incidence of corneal ulceration is reduced.

●In experimental animal studies, inhibitors of collagenase applied topically to the cornea reduced the incidence of corneal ulceration from 80% to 20%. Although both cysteine and acetylcysteine are effective inhibitors of collagenase, the latter is more desirable because of its stability, efficacy, and availability.

●In models of extreme injuries, acetylcysteine has not had any favorable effect. Although it is suspected that 20% acetylcysteine has a favorable effect in the human alkalineinjured cornea, this has not been proved by a randomized clinical trial.

Early insertion of a methylmethacrylate ring designed to fit into the cul-de-sacs might prevent fibrinous adhesions and reduce subsequent fibrotic contracture of the conjunctiva. An alternative approach has been to suture plastic wrap over the palpebral and fornix conjunctiva. Despite such treatments it is not unusual for severely injured eyes to undergo total ankyloblepharon. Later lysis of adhesions with or without mucous membrane grafts, insertion of a symblepharon ring, and placement of intermarginal lid adhesions can restore the cul-de-sacs, improve lid mobility, and reduce or eliminate corneal exposure.

Surgical

Animal studies by Grant have suggested that early paracentesis of the eye does not alter the outcome after an alkaline injury. However, the finding of a severely elevated pH in the aqueous humor of rabbits up to 2 hours after a 2 N sodium hydroxide injury does offer a compelling reason to remove aqueous humor and re-form the anterior chamber with a buffered solution.

●Paracentesis may be safely performed under topical anesthesia by an ophthalmologist.

●A No. 11 Bard–Parker blade can be used initially to facilitate the entry of a 27-gauge needle into the eye.

●If a significant proportion of the perilimbal palisades of Vogt (containing the corneal stem cells) has been destroyed, then a persistent epithelial defect is likely to occur.

●Transplantation of corneal limbal stem cells from the other eye is indicated to stabilize and renew the corneal surface after the episclera has revascularized. (The earliest recorded transplant was performed 2 weeks after injury.)

●To accomplish this, the residual epithelium and pannus, if present, must be removed (lamellar keratectomy), and peritomy with conjunctival recession must be performed to prepare the recipient eye.

●Two or three conjunctival autographs from the uninjured eye, spaced equidistantly around the eye, are delineated with a wet-field cautery 4 mm on a side and excised, including a narrow piece of cornea. The autographs are oriented around the recipient limbus the same way they were in the donor eye and sutured there with 9-0 vicryl.

●In binocular injuries, allografting of corneal stem cells from related or unrelated donors is necessary.

●Corneal stem cell transplantation is required 3 or 4 months before corneal transplantation.

In the acute phase, temporary amniotic membrane patching may be considered.

No medical way is known to reestablish corneal clarity after a moderately severe, severe, or very severe alkaline injury. Extensive scarring and vascularization of the cornea, without other complications, are the best possible outcomes. Corneal transplantation with fresh tissue may be considered no sooner than 12 to 18 months after injury. Such a transplant cannot survive without the normal blink mechanism and an adequate tear film. For this reason, operative procedures to lyse symblephara, expand cul-de-sacs, and eliminate lagophthalmos are often required to reestablish a more normal external anatomy and physiology before transplantation.

The success of corneal transplants in alkaline-injured eyes is steadily improving although they are still regarded as highrisk cases. The high incidence of secondary glaucoma, immunologic rejections, and recurrent epithelial erosions requires continued medical vigilance. Cataract extractions and multiple other procedures often complicate management.

COMPLICATIONS

●Conjunctiva: edema, ischemia, necrosis, scarring, symblepharon.

●Cornea: edema, infiltration, neovascularization, opacity, perforation, ulcer.

●Eyelids: lagophthalmos, scarring.

●Iris or ciliary body: chemical mydriasis, hypopyon, iridocyclitis, ischemic necrosis, phthisis bulbi.

●Other: cataract, secondary glaucoma.

Contusions and152LacerationsCHAPTERConjunctival •

Injuries Nonmechanical and Mechanical • 14 SECTION

TREATMENT

Surgical

Surgical repair is rarely necessary if the laceration is less than 1 cm in length. If surgical reapproximation of a gaping wound is deemed necessary, interrupted or continuous 6-0 or 7-0 gut sutures are sufficient for this purpose. Careful attention should be given to reapproximation of lacerated conjunctival edges in order to exclude Tenon’s capsule from the wound. If Tenon’s fascia is included in a sutured conjunctival laceration, a chalkywhite herniation will result. On rare occasions, extensive loss of conjunctiva may require a conjunctival graft from the other eye or a mucous membrane graft from the mouth. However, even injuries that have resulted in loss of a considerable amount of tissue can usually be closed satisfactorily because of the elasticity of the conjunctiva.

If tissue necrosis has resulted from a severe contusive injury, excision of the necrotic tissue will facilitate more rapid wound healing and will also decrease the possibility of infection.

Supportive

Because conjunctival hemorrhage and chemosis following contusions are usually not serious, treatment requires only supportive therapy such as ice packs to minimize swelling in the acute phase.

Subconjunctival hemorrhage following contusive injuries may at times result in chemosis so severe that the conjunctiva balloons out between the lids. In this situation, treatment does not relieve the edema but may be directed at relief of discomfort. The distended conjunctiva should be covered with ointment or a plastic sheet until the swelling subsides. At some point, the use of a muscle hook may allow an infolding of the conjunctiva into the fornices to a degree that will allow placement of a pressure patch.

Prophylactic use of topical antibiotic solutions is advisable for all conjunctival lacerations.

COMPLICATIONS

●Conjunctival cicatrisation.

●Conjunctival cysts.

●Granulation.

●Keratinization.

●Conjunctival necrosis.

●Pseudomembranous conjunctivitis.

●Symblepharon.

COMMENTS

Most conjunctival wounds involve the bulbar conjunctiva in the interpalpebral zone. Less frequently, the superior and inferior palpebral areas are lacerated, and in these instances, painstaking inspection must be performed. These tears are commonly seen in association with lid lacerations and perforations, and meticulous examination of the underlying sclera and a thorough fundus examination are essential. The possibility of scleral perforation always exists in these cases, and proper management depends on an immediate and accurate diagnosis.

REFERENCES

Norton AL, Green WR: Foreign bodies as a cause of conjunctival pseudomembrane formation. Br J Ophthalmol 55:312–316, 1971.

Paton D, Goldberg MF: Management of Ocular Injuries. Philadelphia, WB Saunders, 1976:181–190.

Rich LF: Conjunctival lacerations. In: Roy FH, ed: Master techniques in ophthalmic surgery. Baltimore, Williams & Wilkins, 1995:97–101.

Runyan TE: Concussive and penetrating injuries of the globe and optic nerve. St Louis, CV Mosby, 1975:1–7.

Williams T, Frankel N: Intracerebral air caused by conjunctival laceration with air hose. Arch Ophthalmol 117(8):1090–1091, 1999.

153 ELECTRICAL INJURY 940.1

(Electric Shock, Lightning)

Frederick T. Fraunfelder, MD

Portland, Oregon

ETIOLOGY/INCIDENCE

Voltages range from that of lightning-up to 100 million volts-to that of electricity. Burns may occur at potentials of less than 6 volts, but significant ocular injuries have not occurred at potentials of less than 200 volts.

The size of a cutaneous burn has a minimal relationship to the long-term outcome. Small skin burns may cause severe multisystem internal injury involving the cardiovascular, central nervous, and musculoskeletal systems. Extensive tissue necrosis and vascular injury can also result from small entry wounds.

Only rarely do lightning injuries cause ocular problems. It is estimated that between 800 and 1000 persons are hit by lightning each year in the United States. About 20% to 30% of these strikes are fatal. Most ocular injuries occur as a result of contact with an electric source. The contact or exit must be on the head, with the current passing through the eye, for ocular damage to occur.

COURSE/PROGNOSIS

Often, the ophthalmologist is not asked to see a patient until long after the injury has occurred because the patient may be severely injured and have ointments covering the face and eyes. Only after the patient improves and ointment is decreased will the patient have visual complaints.

Characteristics of lens changes

●The initial changes that occur in the formation of electric- ity-caused cataracts are multiple vacuoles beneath the anterior lens capsule.

●These vacuoles are replaced by anterior subcapsular ‘streaks’ in an irregular pattern.

●Scale-like gray opacities may appear in the subcapsular layer of the extreme anterior cortex.

●Vesicles and amorphous opacities, as well as crystalline formations, may also appear in the posterior subcapsular area.