Preliminary Planning

Pertinent ocular items in a preliminary medical survey include contact lens wear; previous episodes of nontraumatic iritis; previous episodes of herpetic keratitis; and a history of corneal transplantation, retinal detachment, refractive surgery, or other ocular surgery. A positive response to these questions may alert the health care professional to specific ocular problems that may be encountered on the proposed trip. Congenital color vision deficiencies are common in the male population (8% in whites)³² and typically pose no functional problems in the wilderness.

Ocular health should be reviewed as part of the medical survey, and a basic wilderness eye emergency kit should be assembled and taken on the trip; this is described in the next section.

The Wilderness Eye Emergency Kit

Box 28-1 lists the suggested items for a basic wilderness ocular emergency kit. A topical fluoroquinolone (e.g., moxifloxacin) is the antibiotic eye drop of choice. These medications are preferred for the treatment of bacterial keratitis in a wilderness setting. Topical tetracaine and fluorescein strips are important for diagnosis. Topical prednisolone is an excellent ocular anti-inflammatory medication.

The choice of an oral antibiotic is based on the efficacy of the proposed antibiotic for the treatment of preseptal cellulitis, orbital cellulitis, and penetrating trauma to the globe. The fluoroquinolone family of antibiotics offers several good choices for these indications. The fourth-generation fluoroquinolone moxifloxacin provides good coverage against gram-positive, gram-negative, and anaerobic organisms, with a relatively mild side effect profile and once-daily dosing; it is the recommended first-line oral antibiotic.⁹⁹ Gatifloxacin has recently been withdrawn from the market because of dysglycemic side effects. Trovafloxacin (500-mg tablets) is a systemic fluoroquinolone with excellent coverage against gram-positive, gram-negative, and anaerobic bacteria.^61,138 It offers the convenience of once-daily dosing, but there have been a number of unpublished reports of hepatotoxicity with trovafloxacin that limit the usefulness of this medication.¹⁰⁵ Levofloxacin (500-mg tablets) is a systemic fluoroquinolone with very good activity against a wide variety of gram-positive and gram-negative organisms but less anaerobic coverage than is offered by trovafloxacin.¹⁰⁵ Ciprofloxacin has been shown to have excellent ocular penetration when given orally,⁸⁰ but it is less efficacious against gram-positive organisms than is levofloxacin. Bacitracin is an antibiotic ointment that is suitable for use for patching corneal abrasions. Ophthalmic ointments are best applied with the use of downward pressure on the lower lid to pull it away from the eye followed by the application of a 1-cm (0.4-inch) ribbon of ointment to the conjunctiva of the lower lid. When released, the lid returns to its normal position, and normal blinking distributes the ointment over the corneal surface.

Oral prednisone has at least three possible eye-related treatment uses in the wilderness: (1) refractory iritis; (2) giant cell arteritis; and (3) orbital pseudotumor. Topical scopolamine 0.25% is used to reduce ciliary muscle spasm, which causes much of the discomfort that is associated with iritis and corneal abrasion. However, scopolamine has the disadvantages of dilating the pupil, thus making the eye very sensitive to bright light, and of preventing accommodation, thus making reading very difficult, for 5 to 7 days. Artificial tears are used to treat ocular surface drying and to flush conjunctival foreign bodies from the eye.

Artificial tears are a better choice for these symptoms than are ophthalmic preparations that contain vasoconstrictors, because the latter medications have been shown to cause both acute and chronic conjunctivitis.¹³¹ Diclofenac 0.1% drops have been shown to decrease corneal sensitivity, especially when multiple drops are used.^119,136,137 These drops have been found to be helpful for reducing the discomfort that is associated with traumatic corneal abrasion⁶⁷ and excimer laser refractive surgery.^46,139,144 In the unlikely event of angle-closure glaucoma in a wilderness setting, 2% pilocarpine may be used. The medications in Box 28-1 are listed in my recommended priority order. In the spirit of making do in the wilderness, all of the disorders mentioned in this chapter can be managed with only the aforementioned medications, but alternative therapies are also discussed.

Many individuals suffer from seasonal allergies, including allergic conjunctivitis, and these may be exacerbated in the wilderness. Adding olopatadine 0.1%, lodoxamide 0.1%, nedocromil 2%, or ketotifen 0.025% to the wilderness eye kit provides treatment options for allergic conjunctivitis.⁷⁷ Because this condition is frequently chronic, individuals may carry their own medications on trips.

Visual Acuity Measurement in the Wilderness

Evaluation of visual acuity is an essential element of the eye examination. Serial measurements of visual acuity are used to monitor an individual’s progress while he or she is being treated for infectious, inflammatory, or traumatic eye disorders. Lack of an eye chart does not preclude the ability to obtain a quantitative measurement of visual acuity; rather, a near-vision card can be used for this purpose. Such a card should be held the prescribed distance from the eye; this is usually 35 cm (14 inches). If a near-vision card is not available, the ability to read print in a book is a useful alternative measure. If the individual’s glasses have been lost, use a piece of paper with a pinhole that has been created with the tip of a pen or pencil to help to compensate for the lost refractive correction. Individuals who are 40 years old and older may need a pinhole or reading correction to help them to focus on a near target. Although a marked decrease in visual acuity can be an important warning of a significant ocular disorder, visual acuity cannot always be considered a reliable indicator of the severity of disease. A corneal abrasion victim may initially have worse visual acuity than a person with a retinal detachment or corneal ulcer, despite the fact that the latter two entities are much more serious disorders.

General Therapeutic Approach

The recommendations made in this chapter are not necessarily the preferred management of the disorders mentioned when one is not in the wilderness setting. Of special interest is the recommendation for an individual who is not an ophthalmologist to use a topical steroid for the management of several of the disorders discussed. The use of topical ocular steroids is generally best undertaken by ophthalmologists for two reasons. First, steroids are usually indicated only for relatively serious ocular disorders, which should be followed by an ophthalmologist when possible. Second, topical steroid use may result in elevated intraocular pressure, cataracts, and exacerbation of certain eye infections. All of the disorders for which steroids are recommended in this chapter should be referred to an ophthalmologist for follow up as soon as possible after the patient returns from the wilderness. Caution should be exercised when prescribing a topical steroid for more than 3 days of use. Although cataracts are typically associated with long-term steroid use, a significant rise in intraocular pressure may occur within just a few days after initiation of topical steroid therapy.⁷⁷

The requirement for expedited evacuation is one of the questions that must be answered when treating an eye disease in the wilderness. In the following sections, the need for evacuation may be considered nonurgent unless an emergency (i.e., as soon as possible) or expedited (i.e., as soon as is deemed reasonable given the resources required to accomplish the task) evacuation is specified in the recommendations for treatment.

Acute Periocular Inflammation

Causes of acute periocular inflammation are listed in Box 28-2. The term preseptal cellulitis means that the infectious process is confined to the tissues anterior to the orbital septum. Therefore, preseptal cellulitis manifests as erythema and edema of the eyelids without restricted ocular motility, proptosis, pupillary change, or decrease in visual acuity. However, some of these findings may be difficult to appreciate in the presence of marked lid edema. Historical clues include antecedent periocular trauma or insect bite or sting. Staphylococcus aureus and Streptococcus species are the most common causative organisms in adults.³⁹ In the past, this disorder has been treated very aggressively because of the high incidence of Haemophilus influenzae infection, especially in pediatric patients, with subsequent septicemia and meningitis. The advent of H. influenzae type B vaccine has changed the microbiology of this disorder and may dictate changes in treatment strategies in the future.³⁶ Persons who present with this disorder may be treated with 400 mg of moxifloxacin once a day and should have an expedited evacuation. Alternative antibiotic choices include 500 mg of levofloxacin once a day, 750 mg of ciprofloxacin twice a day, 500 mg of dicloxacillin every 6 hours, or 500 mg of cephalexin four times a day.

Dacryocystitis, which is infection of the lacrimal sac, may mimic the findings of preseptal cellulitis; however, erythema, edema, and tenderness are localized to the area that is inferior to the medial aspect of the eye and over the nasolacrimal sac and duct. The presence of this condition usually indicates an obstruction in the opening between the lacrimal sac and the nasal cavity. Surgical intervention to restore the patency of this opening is usually undertaken after the acute infection is treated. The most common pathogens that cause acute dacryocystitis are S. aureus, Streptococcus species, and, in children, H. influenzae.⁹⁸ Treatment should be initiated with 400 mg of moxifloxacin once a day and warm compresses. Alternative antibiotic choices include 500 mg of levofloxacin once a day, 750 mg of ciprofloxacin twice a day, or 875 mg of amoxicillin and 125 mg of clavulanate every 8 hours. Worsening of the condition after 24 to 48 hours should be managed with an expedited evacuation.

Periocular insect envenomation is a preseptal cellulitis look-alike. Although secondary infection may follow envenomation, the envenomation itself may produce significant erythema and edema. Diagnostic clues include a history of insect bite or a periocular papular lesion at the site of the envenomation. Ice or cool compresses may be used to treat the envenomation, with 400 mg of moxifloxacin once a day, 500 mg of levofloxacin once a day, 500 mg of dicloxacillin every 6 hours, or 500 mg of cephalexin 4 times a day added if secondary infection is suspected.

The term orbital cellulitis means that infection has spread to or originated in the tissues posterior to the orbital septum. This may be manifested as diplopia or restriction in ocular motility as the extraocular muscles are affected, proptosis as edema in the orbit pushes the globe forward, decreased vision as the optic nerve is affected, or pupillary change if innervation of the pupil is affected. Fever is suggestive of orbital cellulitis as part of the differential diagnosis of periocular inflammation. This condition is more commonly associated with sinusitis than with periocular trauma as an antecedent disorder.⁸³ Most series report a 50% to 75% incidence of sinusitis or other upper respiratory infection in association with orbital cellulitis.¹⁴⁶ The bacteria that most commonly cause orbital cellulitis are S. aureus, Streptococcus pyogenes, and Streptococcus pneumoniae.⁹⁸ Anaerobes are frequently present in patients with chronic sinusitis and should be suspected in those with orbital cellulitis that is associated with longstanding sinus disease.⁹⁸ If not treated aggressively, orbital cellulitis may be associated with a life-threatening infection of the central nervous system. Before antibiotics became available, approximately 19% of persons with orbital cellulitis died of intracranial complications, and 20% of survivors became blind in the involved eye.⁹⁸ This disorder requires hospitalization and intravenous antibiotic therapy. Interim therapy should include 400 mg of moxifloxacin once a day. Alternative antibiotic choices are 500 mg of levofloxacin twice a day, 750 mg of ciprofloxacin twice a day, or 875 mg of amoxicillin and 125 mg of clavulanate every 8 hours. A decongestant should be added if sinusitis is present, and emergent evacuation should be undertaken.

Orbital pseudotumor is an inflammatory disease of the orbit that may manifest very much like orbital cellulitis. The differentiation between these two entities may be difficult.⁸³ There would typically not be a history of preceding sinusitis. A reasonable approach in the wilderness is to begin therapy with 400 mg of moxifloxacin once a day and then to arrange for emergent evacuation. Prednisone (80 mg/day) should be added if there is no response to antibiotic therapy, if there is no fever or sign of central nervous system involvement, and if evacuation has not been possible by 24 to 48 hours after presentation. If prednisone therapy is initiated, its efficacy should be evaluated after 48 hours. If there has been a decrease in pain, erythema, edema, or proptosis, therapy should be continued until evacuation is accomplished. If there has been no response after 48 hours, the prednisone may be discontinued without tapering.

Periocular Trauma

Retrobulbar Hemorrhage

Blunt or penetrating periocular trauma may result in orbital bleeding. If the bleeding is contained by the orbital septum, an orbital compartment syndrome may ensue. Because the pressure in the orbital compartment is progressively elevated, intraocular pressure will also rise. If intraocular pressure rises to a high-enough level, either central retinal artery occlusion or damage to the optic nerve may ensue, and vision may be permanently lost in the eye. Signs and symptoms of retrobulbar hemorrhage include pain, periorbital ecchymosis, progressive proptosis (i.e., bulging forward of the eye), decreased vision, diffuse subconjunctival hemorrhage, and an afferent pupillary defect. Definitive management of this disorder is a minor surgical procedure called lateral canthotomy (Figure 28-1) in which an incision is made at the lateral aspects of the eyelids to relieve pressure in the orbit.

FIGURE 28-1 Lateral canthotomy and inferior cantholysis are indicated for casualties that manifest with orbital hemorrhage and evolving orbital compartment syndrome. Step 1, Infiltrate the lateral canthal area with a local anesthetic (e.g., 2% lidocaine with epinephrine) and use tetracaine drops in the eye for topical anesthesia. Step 2, Place a mosquito clamp on the lateral canthus that extends horizontally toward the orbital rim for a distance of 1 cm. Leave it in place for 30 seconds to assist with hemostasis. Step 3, Remove the clamp, and use a pair of fine (e.g., Stevens) scissors to divide the lateral canthal tissues along the line created by the clamp. This completes the lateral canthotomy. Step 4, Next, use the scissors to cut the inferior crus of the lateral canthal ligament. Position the scissors perpendicular to the canthotomy incision that was made in Step 3 (i.e., not along the lid margin), and cut the ligament. This completes the inferior lateral cantholysis. Step 5, The completed lateral canthotomy and cantholysis are shown. These procedures allow the orbital tissues to move forward slightly, and they help to relieve the pressure in the orbital compartment.

Chemical Injury of the Eye

The mainstay of management of any chemical eye injury is immediate and copious irrigation of the ocular surface with water from whatever source is most readily available. Lactated Ringer’s solution or normal saline is the preferred irrigation fluid, when available³⁹; however, in the wilderness, bottled water may be the best option. If none of these fluids is available, treated (i.e., filtered and disinfected) water from a drinking container is the next best option, with untreated water being the last resort. Instillation of several drops of tetracaine will make the procedure much less uncomfortable for the victim. Irrigation should be continued for a minimum of 30 minutes.⁸³ The two most damaging chemicals are strong acids and alkalis.⁸³ Sulfuric acid from an exploding car battery is a typical acid, whereas cleaning products (e.g., drain cleaners) are typical alkalis. Caustic alkalis are more likely to damage the eye than are acids because of their profound and rapid ocular penetration. Do not attempt to neutralize the corneal surface with acidic or alkaline solutions. Chemicals other than acids and alkalis may be uncomfortable when they are encountered, but they are less likely to produce significant long-term damage.

After a minimum of 30 minutes of flushing has been completed, the eye should be examined for retained particles; these should be removed with a moistened cotton-tipped applicator.⁸³ Treatment for an acid- or alkali-induced injury includes moxifloxacin 0.5% drops (one drop four times a day) or bacitracin ointment every 1 to 2 hours while awake until fluorescein staining confirms that the corneal epithelial defect that typically accompanies these injuries has resolved. Topical prednisolone 1% should be added if there is significant inflammation. Prednisolone drops should be used every hour while awake for 3 days. Eye pain is managed with scopolamine drops four times a day for 3 days and oral pain medications.¹²¹ Frequent use of artificial tears may also help to relieve discomfort. Evacuation should be expedited if the cornea is found to be opaque, if a large epithelial defect is found on fluorescein staining, or if significant pain persists after 3 days. Another sign of serious injury is blanching of the conjunctiva in the limbal area.⁸³

A special type of chemical injury to the eye is ocular envenomation from a spitting cobra.^51,56,141 Ocular injury from cobra venom may be severe and result in blindness. Cobras can project this venom out to a range of 3 m (10 feet), and they typically aim directly for the victim’s eyes. Ocular surface envenomation causes severe conjunctival and corneal inflammation, edema, and erosions. Corneal erosions may progress to corneal ulceration, perforation, hypopyon, and endophthalmitis. Central corneal opacification may result despite aggressive therapy. One report described nine individuals who had suffered ocular surface cobra envenomations.¹⁴¹ Five had only severe conjunctivitis; corneal erosions developed in the other four. Two individuals were permanently blinded as a result. Therapy includes immediate flushing of the eyes as described previously. After this is done, check for a corneal abrasion, and treat it with moxifloxacin 0.5% drops if an erosion is present (one drop four times a day until the erosion is healed). Note that healing may be prolonged in toxin-induced corneal surface injuries. Immediate consultation with a toxicology consult service and a corneal or external disease subspecialist should be obtained, if possible, and an expedited evacuation should be arranged. Topical steroid therapy should be considered (one drop of prednisolone every hour while awake) and discussed with the consultant. The decision to treat is based on the severity of symptoms and the presence or absence of a corneal erosion or ulcer. The value of the topical application of specific cobra antivenom has not been documented, so this therapy is not recommended. Systemic heparin therapy has been shown to be useful for prevention of corneal opacification in animal models of this injury.^64,65

Another type of chemical injury of the eye may occur when the eyes are sprayed with skunk musk. Such an episode should be managed with immediate ocular irrigation as described previously. If discomfort persists beyond several hours, check for a corneal abrasion, and treat this with moxifloxacin 0.5% drops (one drop four times a day until the abrasion is healed). If fluorescein staining does not show an abrasion but significant discomfort persists, a 3-day course of prednisolone 1% drops (one drop four times a day for 3 days or until symptoms have resolved) may be of benefit. If pain is severe and unrelieved by prednisolone drops or if it persists after the 3-day course has been completed, consider an expedited evacuation and an ophthalmologic consultation.

Acute Loss of Vision in a White, Quiet Eye

Vision may be variably decreased with many of the disease entities that are noted in the section about Acute Red Eye, later. The current section addresses sudden loss of vision that occurs in a white, quiet eye. A differential diagnosis is provided in Box 28-3. Disorders that cause this symptom are often difficult to diagnose without ophthalmic instruments, none of which is included in the kit described in Box 28-1. There are few treatments for most of these disorders that are likely to be effective in a wilderness setting. Although an afferent pupillary defect (e.g., Marcus Gunn pupil) may be present, this is a nonspecific finding that would be expected with most of the disorders listed in Box 28-3, except for vitreous hemorrhage and high-altitude retinal hemorrhage.

An important question that must be asked in the face of acute loss of vision in a white, quiet eye is “Does this person have giant cell arteritis?” Giant cell arteritis (GCA), which is also called temporal arteritis, can cause devastating anterior ischemic optic neuropathy that is often first noted on waking and that usually becomes permanent.⁴⁹ Subsequent involvement of the second eye is common if GCA in the first-stricken eye is not promptly treated.⁴⁹ Although visual loss has been reported to occur in both eyes simultaneously, there is typically a delay of 1 to 14 days before the second eye is affected.¹ Loss of vision in the second eye can be prevented in most cases by prompt initiation of high-dose corticosteroid therapy.^1,49,59,104

Arteritic anterior ischemic optic neuropathy is typically a disease of older individuals, with one large study reporting a mean age of onset of 70 years and the age of the youngest patient as 53 years.¹ Clues to diagnosis are temporal headache, jaw claudication, fever, weight loss, transient visual obscurations, and polymyalgia rheumatica (i.e., generalized myalgias).¹⁰⁴ The visual obscurations seen with GCA usually last for 2 to 3 minutes.¹⁰⁴ If a person is thought to be suffering from GCA, he or she should be started on 80 mg of prednisone once a day, and evacuation should be expedited. If prednisone or steroids of equal or greater systemic potency are not available, then the evacuation should be considered an emergency.

If one suspects that loss of vision is the result of retinal detachment on the basis of a history of high myopia (i.e., extreme nearsightedness), floaters, or photopsias (i.e., flashing lights), expedited evacuation should be undertaken because of the need for surgical repair. Loss of central vision caused by a retinal detachment usually means that the macula is involved and that surgical repair is urgent rather than emergency. Ross and Kozy¹¹⁶ found that a delay to surgery of up to 1 week in macula-off rhegmatogenous retinal detachments did not affect final visual acuity. Expedited evacuation to a facility that has retinal surgery capability allows for more precise determination of the urgency for surgical repair. The presence of “floaters” in the field of vision is a very common occurrence among individuals who are middle aged or older. An acute awareness of floaters may be caused by certain activities, such as looking at a visually homogenous background (e.g., the sky). If the floaters are new in onset or suddenly more numerous than before or if they are accompanied by a sensation of flashing lights (i.e., photopsias), this suggests the possibility of posterior vitreous detachment (PVD), which is detachment of the vitreous face from the retina. PVDs are common, and they are usually not a problem, except for the annoying floaters; however, the suspicion of PVD should prompt a visit to the ophthalmologist as soon as is practical so that he or she can check to make sure that the PVD has not caused a retinal tear or detachment. Expedited evacuation from the wilderness environment is not required for floaters alone.

If the victim is at a high altitude (i.e., >3048 m [10,000 feet]), high-altitude retinal hemorrhage, which is discussed later in this chapter, should be suspected; further ascent should be avoided.¹⁹ Descent of at least 915 m (3000 feet) should be undertaken as soon as is feasible.¹⁹

Another potentially treatable cause of sudden loss of vision in a white, quiet eye is central retinal artery occlusion (CRAO). Previous conventional therapy for CRAO of ocular massage, pentoxifylline, and anterior chamber paracentesis has been reported to be unsuccessful for restoring the vision in 40 of 41 patients with CRAO, even though 11 patients presented within 6 hours of visual loss and 17 patients presented within 12 hours.¹¹⁷ Primate retinas can tolerate no more than 100 minutes of ischemia caused by complete blockage of retinal blood flow.⁵⁸ However, fluorescein angiography has shown that in humans CRAO is seldom complete and that therapy begun up to 6 hours after visual loss may be successful for restoring vision.¹¹⁷

Hyperbaric oxygen was reported to be successful for restoring vision on two separate occasions in one patient with recurrent branch retinal artery occlusions that were associated with Susac’s syndrome.⁸¹ Oxygen is supplied to the retina from both the retinal and choroidal circulations. Under normoxic conditions, approximately 60% of the retina’s oxygen is supplied by the choroidal circulation. Under hyperoxic conditions, the choroid is capable of supplying 100% of the oxygen required by the retina.⁸¹ When retinal arterial flow is interrupted, the retinal tissue undergoes a period of ischemia. Blood flow may be spontaneously reestablished, which frequently happens with arterial obstruction, or ischemia may continue until cell death and necrosis occur.⁸⁷ The period of time during which the tissue is ischemic yet still capable of recovery is called the ischemic penumbra.⁸⁷ Hyperbaric oxygen is not always required for a reversal of retinal ischemia. The author has treated a monocular patient who suffered CRAO in his only seeing eye and presented to the emergency department within an hour of visual loss. The victim’s vision improved from 20/400 to 20/25 within minutes after he received supplemental oxygen by mask. Unfortunately, however, his vision decreased rapidly to 20/400 whenever the supplemental oxygen was removed. The victim was heparinized and maintained on supplemental oxygen for approximately 10 hours, at which time the removal of oxygen no longer caused a decrease in vision. If oxygen is being carried for an extreme altitude summit attempt or for other purposes, a person with sudden painless loss of vision should be given a trial of oxygen administered in as high a concentration as possible to see if this therapy results in visual improvement. CRAO has been approved by the Undersea and Hyperbaric Medical Society as an indication for hyperbaric oxygen therapy.⁹⁴ Other ocular indications for hyperbaric oxygen therapy have been summarized in a recent review article²³ and textbook chapter.²⁵ Ocular contraindications to and complications of hyperbaric oxygen therapy have also been recently summarized.²²

Care should be taken when monocular visual loss occurs. Although central vision may still be normal in the fellow eye, depth perception may be impaired, and the victim may therefore be at increased risk of a fall during evacuation.

Acute Red Eye

Box 28-4 provides a partial list of disorders that can result in an acute red eye. In the absence of a slit lamp, the diagnosis must rely on the basic techniques of history, penlight inspection, fluorescein staining, response to administration of topical anesthesia, and pupillary status. The discussion of the differential diagnosis of the acute red eye that follows makes use of these clinical findings to establish the diagnosis. An algorithmic representation is shown in Figure 28-2. The term fluorescein positive is used to denote an eye with a discrete area of staining noted with cobalt blue light after instillation of fluorescein dye. Some conditions, such as blepharitis, viral keratoconjunctivitis, and ultraviolet (UV) keratitis, may cause a pattern of punctate staining that is referred to as superficial punctate keratitis (SPK).

FIGURE 28-2 Algorithm that shows the wilderness diagnostic procedure for the acute red eye.

Traumatic Ocular Disorders

Obvious Open Globe

If there is a history of trauma and if penlight inspection of the eye reveals an obvious open globe (e.g., the eye in Figure 28-3), the examination should be discontinued and a protective rigid shield placed over the eye. Do not apply a pressure patch or instill any topical medication. There are two primary concerns during management of this condition. The first is to minimize manipulation or additional trauma to the eye that might raise intraocular pressure and result in expulsion of intraocular contents through the corneal or scleral defect. The second is to prevent development of post-traumatic endophthalmitis, which is an infection of the aqueous and vitreous humors of the eye. This typically has devastating visual results, with only 30% of victims in one study retaining visual acuity that is greater than or equal to 20/400.⁷⁶ Staphylococcus epidermidis is the most common pathogen that is implicated in this condition, but Bacillus cereus is a very aggressive pathogen that is also often isolated.⁷⁶ After the shield is placed, the victim should be started on 400 mg of moxifloxacin once a day or 500 mg of levofloxacin once a day; 750 mg of ciprofloxacin twice a day is another option. Penetration of antibiotic into the vitreous cavity is of major concern with penetrating eye trauma, so other antibiotics should not be substituted unless they are known to have adequate vitreal penetration. A person with an obvious open globe requires surgical repair as soon as possible and should be evacuated as an emergency. Because there is a possibility that air may have been introduced into the eye, barometric pressure changes during evacuation should be minimized, if possible. However, this consideration is secondary to the need for expeditious transport to a facility where surgical repair can be performed. Emesis should be treated or prevented if antiemetic medications are available. The need for surgical intervention shortly after arrival at the hospital should be anticipated. The victim should not be allowed to become dehydrated as a result of a prolonged evacuation time from the wilderness setting, so plain water by mouth may be allowed up to several hours before arrival at the hospital.

FIGURE 28-3 Obvious open globe (i.e., corneoscleral laceration).

(Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

Occult Ruptured Globe

A penetrating injury to the eye or a ruptured globe may not always be obvious. Clues to occult rupture include large subconjunctival hemorrhage with chemosis; dark uveal tissue that is present at the limbus; distorted pupil (Figure 28-4); fluorescein leak from a linear or punctate corneal epithelial defect; mechanism of injury (e.g., hammering metal on metal, impaling injury); or a decrease in vision. If an occult globe rupture is suspected, the victim should be treated as described previously for an obvious open globe. The relatively less severe appearance of the injury does not eliminate the threat of endophthalmitis, so systemic antibiotic therapy as noted previously should be initiated. Snakebite injuries to the eye are thankfully uncommon, but they may result in occult open globe injury as a result of penetration by teeth or fangs.⁵ If the snake is venomous, direct injection of toxin into the globe has been reported to cause necrosis, uveitis, and keratomalacia. Another type of penetrating ocular injury particular to the wilderness environment is injury to the eye from a fishhook that has become embedded in the globe or in the periocular tissues. Principles of management include protecting the eye from further injury by covering it with a shield, avoiding manipulation of the hook that may worsen known or suspected injury to the globe, beginning systemic antibiotics as soon as possible, and expediting evacuation of the victim to the care of an ophthalmologist.

FIGURE 28-4 Occult open globe with uveal pigment at the limbus and a peaked pupil.

(Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

Corneal Abrasion

A corneal abrasion is disruption of the protective epithelial covering of the cornea (Figure 28-5). This results in intense pain, tearing, light sensitivity (i.e., photophobia), and increased susceptibility to infection until the defect has healed, usually in 2 to 3 days. There is typically a history of antecedent trauma or contact lens wear. The sine qua non for this diagnosis is an epithelial defect on fluorescein staining. Standard treatment in the recent past consisted of antibiotic ointment followed by application of a pressure patch. A study showed that small (<10 mm²) and noninfected abrasions that were not related to contact lens wear healed significantly faster with less discomfort when they were not patched.⁶⁹ Standard texts now note that patching is rarely used.³⁹ In a wilderness setting, the nonpatching option has the additional advantages of not rendering the victim completely monocular and of not adversely affecting visual field and depth perception. If the nonpatching option is chosen, the victim should be treated with moxifloxacin 0.5% drops (one drop four times a day) or bacitracin ointment four times a day until the corneal epithelium is healed. Diclofenac drops four times a day should be helpful for reducing discomfort. Sunglasses may help to alleviate photophobia. Repeated use of a topical anesthetic for pain control is contraindicated. If the abrasion is contact-lens related, the eye should not be patched because of the increased risk of corneal ulcer that is present with a contact-lens–related abrasion;¹¹¹ contact-lens–related corneal abrasions should be treated with moxifloxacin 0.5% drops (one drop every 2 hours while awake) until the epithelial defect has resolved. An abrasion that is associated with vegetable matter should also not be patched.¹¹¹ If the abrasion is large or if the victim’s discomfort is severe, scopolamine drops once or twice a day may be added to the antibiotic (wait 5 minutes between each drop). Much of the pain that is associated with corneal abrasion and ulcer is the result of ciliary muscle spasm, which is relieved by scopolamine. The rationale for using scopolamine only with a very painful abrasion in the wilderness is that this medication will cause the pupil to dilate (and the eye to become very sensitive to light) and lose accommodation (with a resultant decrease in near visual acuity) for approximately 5 to 7 days. Contact lenses should not be worn until the abrasion has resolved.³⁹

FIGURE 28-5 Corneal abrasion.

(Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

An oral analgesic may be required for pain control. The victim should be monitored daily for development of a corneal ulcer, which is noted on penlight examination as a white or gray infiltrate on the cornea, and for progress in healing of the epithelium as measured by the resolution of fluorescein staining.

Corneal Ulcer

The term corneal ulcer, as used in this chapter, denotes acute bacterial, fungal, or protozoal infection of the cornea. Chronic corneal epithelial defects caused by a variety of autoimmune or inflammatory processes are also referred to with this term at times, but these disorders are beyond the scope of this chapter. Although a corneal ulcer (Figure 28-6) is an infectious process, it is often preceded by a traumatic corneal abrasion. The other predisposing condition for a corneal ulcer is contact lens wear, which results in microtrauma to the corneal epithelium and may allow bacteria or other microorganisms to infect the cornea. Corneal ulcers are typically significantly painful. A small white or gray infiltrate on the cornea can be appreciated by a careful penlight examination. If it is not treated aggressively, the small initial lesion may progress to the much larger infiltrate (see Figure 28-6), with a correspondingly more severe impact on visual acuity. Fluorescein staining reveals an epithelial defect overlying the infiltrate. The associated pain is usually significantly decreased by applying a topical anesthetic, but ciliary spasm may cause pain relief to be incomplete.

FIGURE 28-6 Corneal ulcer.

(Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

An inadequately treated corneal ulcer may result in visual loss from dense corneal scarring or ocular perforation with subsequent endophthalmitis. Management of this disorder in the past included hospital admission for treatment with concentrated and frequently administered aminoglycoside and cephalosporin topical drops. Outpatient therapy with fourth-generation fluoroquinolone eye drops has been shown to be comparable in efficacy with fortified antibiotic preparations.^63,100 Thus, treatment for corneal ulcer should be with moxifloxacin 0.5% drops as follows: one drop every 5 minutes for five doses initially, then one drop every 30 minutes for 6 hours, and then one drop every hour thereafter around the clock.¹¹¹ One drop of scopolamine given two to four times a day may help to relieve the discomfort that is caused by ciliary spasm. Repeated use of topical anesthetics for pain control is contraindicated. Moxifloxacin (400 mg by mouth once a day) may be added if evacuation is delayed and either the infiltrate or the victim’s pain is becoming worse.³⁹ Systemic analgesia may be required if pain is severe. Expedited evacuation and immediate evaluation by an ophthalmologist are recommended.

Traumatic Iritis

The term iritis refers to inflammation of the iris or, more accurately, of the anterior uveal tract of the eye; it may also be called anterior uveitis or iridocyclitis. The defining feature of this condition is inflammatory cells in the anterior chamber of the eye, which must be visualized with a slit lamp. In the wilderness, this diagnosis must be presumptive. Iritis may accompany a corneal abrasion, or it may result from blunt trauma. The diagnosis rests primarily on the presence of significant post-traumatic pain without a corneal abrasion or ulcer noted on fluorescein staining or on pain that persists after the abrasion is healed. Treatment is with one drop of prednisolone four times a day for 3 days. One drop of scopolamine twice a day may be added if pain is severe enough to justify the blurred vision that results from this therapy. Expedited evacuation should be undertaken if severe pain persists.

Subconjunctival Hemorrhage

Subconjunctival hemorrhage (Figure 28-7) is a bright red area over the sclera of the eye that results from bleeding between the conjunctiva and the sclera. It is easily visible without the use of a slit lamp. This injury is innocuous and resolves over a period of several days to several weeks without treatment. In the presence of antecedent trauma, one should be alert for another more serious injury. In particular, if hemorrhage results in massive swelling of the conjunctiva (i.e., chemosis), then an occult globe rupture should be suspected.

FIGURE 28-7 Subconjunctival hemorrhage.

(Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

Hyphema

The term hyphema is defined as blood in the anterior chamber. Although this is usually seen in the setting of acute trauma, it may also be caused by other conditions, such as iris neovascularization. The eye should be examined with the victim sitting upright. If enough blood is present, it collects at the bottom of the anterior chamber and is visible as a layered hyphema (Figure 28-8). This may not be appreciated if the victim is examined while in a supine position or if the amount of blood is very small.

FIGURE 28-8 Hyphema.

(Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

Although most hyphemas resolve without sequelae, this disorder may be complicated by an acute rise in intraocular pressure or corneal blood staining. Treatment in the wilderness consists of activity restriction (i.e., walking only), prednisolone drops four times a day, avoidance of aspirin or nonsteroidal anti-inflammatory drugs, and use of a rigid eye shield until the hyphema has resolved. Do not use a pressure patch. Diamox (250 mg four times a day by mouth) should be added, if available, to treat potentially increased intraocular pressure. The victim should be maintained in a head-up or head-elevated posture, if possible, to promote settling of the hyphema and clearing of vision. Pain should be managed with acetaminophen or another analgesic medication that does not impair platelet function. Retinal injury or an occult ruptured globe may accompany traumatic hyphema. A hyphema victim requires ophthalmologic evaluation, so expedited evacuation should be undertaken. If a hyphema victim experiences improvement of vision followed by a sudden worsening of vision, this may indicate that a rebleed or retinal detachment has occurred, and emergency evacuation should be considered.

Nontraumatic Fluorescein-Positive Acute Red Eye

Herpes Simplex Virus Keratitis

The essential element in this diagnosis is the characteristic dendritic epithelial pattern on fluorescein staining (Figure 28-9). There will often be a history of previous episodes of herpes simplex virus keratitis. Treatment is with trifluridine 1% drops nine times a day.¹¹¹ Treatment is continued until the corneal staining has resolved, at which time the frequency of dosing is reduced to four times a day for 1 week. Trifluorothymidine was not included in the list of eye medications to be taken on the expedition because trifluorothymidine drops require refrigeration. If a significant delay is anticipated before evacuation, herpes simplex virus keratitis may be treated by giving three to five drops of tetracaine 1 minute apart to anesthetize the cornea and then performing a gentle cotton-tipped applicator debridement of the epithelial lesion.¹¹¹ The resulting epithelial defect should then be treated as described previously in the Corneal Abrasion section.

FIGURE 28-9 Herpes simplex virus keratitis.

(Courtesy Steve Chalfin, MD, University of Texas Health Science Center, San Antonio, Tex.)

Corneal Erosion

A corneal erosion is an epithelial defect that is caused by nontraumatic disruption of the corneal epithelium. The fluorescein staining pattern seen with corneal erosion may be identical to that seen with corneal abrasion; pain and photophobia are present with both disorders. The diagnosis is made when the apparent corneal abrasion has no history of trauma to explain its presence. There is often a history of previous similar episodes. The two primary causes of corneal erosion are corneal dystrophies and previous ocular trauma.¹⁰⁴ Recurrent corneal erosions are believed to be caused by a defect in healing between the hemidesmosomes of the corneal epithelium and the underlying basement membrane.⁸³ At night, the epithelium may become adherent to the closed eyelid during sleep. When the individual awakens and opens his or her eyes, the corneal epithelium is pulled away from the basement membrane by movement of the lid; this accounts for the typical history of acute onset of pain on awakening. Signs and symptoms include red eye, pain, tearing, foreign-body sensation, and usually an epithelial defect, although this may be a variable sign, depending on when the patient is evaluated.⁸³

Treatment of these lesions may be difficult. The cornea should be inspected for a loose sheet of epithelium that remains partially attached to the corneal surface. If this is present, try to debride it with a cotton-tipped applicator after topical anesthesia with tetracaine. The lesion is then managed initially in the same manner as a corneal abrasion. There is a high rate of recurrence if follow-up treatment with 5% sodium chloride ointment each evening or anterior stromal puncture is not undertaken.

Corneal Abrasion and Corneal Ulcer With Contact Lens Wear

Both corneal abrasions and corneal ulcers may occur as complications of contact lens wear; management of these conditions has been described earlier. Contact-lens–related corneal abrasions have a relatively high incidence of progressing to corneal ulcers.⁶⁹ Therefore, they should not be patched, and should receive topical antibiotic therapy with moxifloxacin 0.5% drops every 2 hours while awake until the epithelial defect has resolved. Contact lens wear in both eyes should be discontinued immediately. If an ulcer is related to contaminated lens solutions, infection in the first eye may be followed rapidly by a similar occurrence in the other eye.

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