A resource for students of Survive First Aid Training Skip to content
Survive Student Resource

Wilderness Medical Society Practice Guidelines for Treatment of Eye Injuries and Illnesses in the Wilderness: 2014 Update

Wilderness Medical Society

Ryan Paterson, MD; Brandy Drake, MD; Geoffrey Tabin, MD; Frank K. Butler Jr, MD; Tracy Cushing, MD, MPH

From the Kaiser Permanente Medical Group—Colorado (Dr Paterson); the Valley View Hospital Glenwood Springs, CO (Dr Drake); the Denver Health Medical Center/University of Colorado School of Medicine, Denver, CO (Drs Paterson and Cushing); the University of Utah School of Medicine, Salt Lake City, UT (Dr Tabin); and the US Army Institute of Surgical Research, Committee on Tactical Combat Casualty Care, Defense Board, Fort Sam Houston, TX (Dr Butler).

A panel convened to develop an evidence-based set of guidelines for the recognition and treatment of eye injuries and illnesses that may occur in the wilderness. These guidelines are meant to serve as a tool to help wilderness providers accurately identify and subsequently treat or evacuate for a variety of ophthalmologic complaints. Recommendations are graded on the basis of the quality of their supporting evidence and the balance between risks and benefits according to criteria developed by the American College of Chest Physicians. This is an updated version of the original guidelines published in Wilderness & Environmental Medicine 2012;23(4):325–336.

Introduction

Although eye complaints constitute approximately 3% of visits to emergency departments each year, their incidence in the wilderness is unknown.1 Eye problems in the wilderness represent a challenging group of complaints for several reasons: access to proper equipment is limited, access to proper medications may be limited, and most practitioners in the wilderness are not specially trained.2 The Wilderness Medical Society (WMS) published a set of guidelines on eye injuries in the wilderness in 2001. A panel was convened at the WMS Mountain Medicine meeting in Park City, UT, in February 2011 to update those guidelines with the most relevant evidence-based information.

Methods

The panel was convened at the 2011 Wilderness and Mountain Medicine WMS conference in Park City, UT. The WMS members were selected on the basis of clinical interest, research experience, or ophthalmologic expertise. Relevant articles were identified through the PubMed and Cochrane Collaboration databases using keyword searches with the appropriate terms corresponding to each topic. Studies were reviewed, and the level of evidence was assessed. Data regarding specific wilderness treatment of eye injuries are sparse; therefore, we evaluated the data regarding eye injuries and illness in general and adapted these to the wilderness setting. The panel used a consensus approach to develop recommendations regarding diagnosis, treatment, and prevention of ocular injuries in the wilderness. These recommendations have been graded on the basis of clinical strength as outlined by the American College of Chest Physicians (ACCP) (see online Supplementary Table 1) and in conjunction with prior WMS practice guidelines.3

EXAMINATION AND EQUIPMENT

Examination of the eye in the wilderness may be difficult owing to lack of specialized equipment, but many basic elements of the eye examination can be completed in austere settings. The Table provides a list of equipment and medications that should be included in both a basic and an advanced eye kit. A basic kit is appropriate for short excursions, whereas the basic plus the advanced kit could be used for prolonged expeditions, especially to remote locations.

PRE-TRIP PLANNING AND PREVENTION

All people who have a history of any ophthalmologic problems who are participating in wilderness activities should have a complete eye examination within 3 months of any extended trip. Participants should be encouraged to bring all of their own equipment and medications, including glasses, goggles, sunglasses, contacts, lens solution, and any specific medications that they are currently taking or anticipate requiring. Additionally, participants should bring a copy of their lens prescription to aid in the acquisition of new corrective wear if needed or simply bring extra glasses or contacts if they will be in austere settings. Prevention of eye illness and injuries is paramount. Many eye illnesses are a result of accident, and thus may not be preventable, yet adequate sun and protective eyewear, good hygiene, and proper hand washing can prevent a large number of the conditions addressed in these guidelines.

Medical Eye Complaints

ACUTE VISION LOSS IN THE WHITE EYE

Vision loss can occur in both the red and white eye. As these are quite rare, data on these illnesses in the wilderness are very limited; therefore, wilderness management is adapted from clinic or hospital treatments to the wilderness setting as appropriate. There are numerous causes of acute vision loss; regardless of the cause, any vision loss should be considered an emergency, and all patients with vision loss should be considered for emergent evacuation (see the Table).

CENTRAL RETINAL ARTERY OCCLUSION

Central retinal artery occlusion (CRAO) is an ischemic stroke of the retina, usually as a result of an embolic event, that causes abrupt vision loss.4 Treatment options in the wilderness are limited, but there are case reports to suggest improvement in visual acuity after providing highflow oxygen.5 There are also several case studies that report improvement with hyperbaric oxygen therapy. Central retinal artery occlusion is currently an approved indication for hyperbaric oxygen therapy by the Hyperbaric Oxygen Committee of the Undersea and Hyperbaric Medicine Society.5 If oxygen or hyperbaric therapies are available, they should be strongly considered for patients with suspected CRAO. Although a 2009 Cochrane Review found 2 randomized controlled trials evaluating 2 potential treatments for CRAO, pentoxifylline tablets and enhanced external counterpulsation, both trials showed improved retinal artery flow with their treatments, but neither showed improvement in vision.6 These treatments are not available in the wilderness. Evacuation of these patients should be emergent.

  • Oxygen:1C
  • Hyperbaric oxygen therapy:1C
  • External counterpulsation:2B
  • Pentoxifylline:2B
  • Emergent evacuation: 1C

Table - basic and advanced equipment and medications

Basic equipmentBasic medications
Light source: ideally would be penlight with blue filter, but bright headlamp is reasonable optionArtificial tears, individual bullet packs to avoid contamination
Cotton-tipped applicatorsFluorescein strips
Paperclip for lid retractionErythromycin ophthalmic 0.5% ointment
Proparacaine 0.5% drops
Oral pain medicine
Advanced equipmentAdvanced medications
Metal eye shield: can be improvised from anything that will protect eye from further damageFluoroquinolone ophthalmic eye drops, such as moxifloxacin 0.5%
Magnifying glassPrednisolone 1% drops
Fine forcepsMoxifloxacin 400-mg tablets
Small needle, such as 23G or tuberculin syringePrednisone 20-mg tablets
Direct ophthalmoscopeAtropine ophthalmic 1% ointment
Wire speculum for lid retractionPilocarpine 2% drops
Diamox oral 250-mg tablets
Topical NSAID, such as ketorolac, diclofenac, or bromfenac eye drops
  • Equipment: 1C; medications: 1C.

NSAID, nonsteroidal anti-inflammatory drug.

CENTRAL RETINAL VEIN OCCLUSION

Central retinal vein occlusion (CRVO) is a blockage of the venous outflow from the eye leading to profound, painless vision loss. It can be a result of a thrombus, external compression, or vasculopathy, and usually occurs in people older than 50 years who have hypertension.7 Patients with CRVO will usually have an afferent pupillary defect4 : when a light is shone in the normal eye, both pupils will constrict, but when the light is then quickly shone in the abnormal eye, both pupils will dilate. It should be noted that many diseases that cause a unilateral optic neuropathy or retinal problem (such as ischemic optic neuropathy, retinal detachment, and CRVO) can lead to an afferent pupillary defect. It is not necessarily important to differentiate these conditions, but to recognize this abnormal finding. Although the treatments of CRVO in the hospital are complicated and involve laser treatments and intravitreal steroid administration, it is nevertheless reasonable to start treatment in the wilderness with topical steroids, if available (prednisolone 1%, 2 drops in the affected eye 4 times daily). Evacuation should be emergent, as these patients need specialist care and treatments.

  • Topical steroid:1C
  • Emergent evacuation:1C

RETINAL DETACHMENT

A retinal detachment is characterized by vision loss or floaters and flashes of bright light in a patient’s visual field. The vision loss is often described as a fixed cloudy or curtains like defect in the visual field. This condition is usually painless. Visual loss is variable, depending on where on the retina the tear has occurred.4 These patients should be emergently evacuated, as surgical management may be necessary, and there is no effective field treatment.

  • Emergent evacuation:1C

PERIOCULAR INFLAMMATION

Inflammation of the periocular region includes preseptal cellulitis, orbital cellulitis, and dacrocystitis. Preseptal cellulitis is an infection limited to the space anterior to the orbital septum, which includes the superficial tissue surrounding the eye and the eyelids. Orbital cellulitis is more extensive and involves the soft tissues in the bony orbit (deep to the orbital septum). Clinically, preseptal cellulitis presents with swelling and inflammation of the eyelid without involvement of the eye itself. Orbital cellulitis presents with inflammation within the orbit, including bulging of the eye (proptosis), swelling of the conjunctiva (chemosis), painful extraocular movements, and possible visual disturbance.8 Additionally patients with orbital cellulitis may be systemically ill and have a fever. Periorbital cellulitis, while isolated to the preseptal space, is often associated with marked swelling, which makes the differentiation of preseptal from orbital cellulitis difficult. Preseptal cellulitis can be caused by spread from sinusitis, conjunctivitis, or blepharitis. Causes that may be more commonly encountered in the wilderness include trauma and insect bites.8 Orbital cellulitis is usually caused by a sinus infection.9 Additionally, preseptal cellulitis can spread and cause orbital cellulitis. There are limited data regarding management of these entities in the wilderness. Rapid identification of orbital cellulitis is paramount, as orbital cellulitis is a true medical emergency. Failure to treat this infection quickly can lead to blindness, intracranial infection, and possibly death. Initial management of both conditions requires antibiotics that cover Staphylococcus aureus, Streptococcus pneumoniae,and Haemophilus influenzae.8

Consideration should also be given toward coverage of anaerobes and methicillin-resistant S aureus(MRSA).9 Treatment of both preseptal and orbital cellulitis should begin with amoxicillin/clavulanate 875 mg orally, 2 times daily for 10 days, but if that is not available, then oral fluoroquinolones (such as moxifloxacin) may be substituted.10 If the practitioner is certain that an infection is isolated to the preseptal space, evacuation can be nonemergent. However, if there is any question that the infection may involve the orbit, or a presumed preseptal cellulitis is not responding to antibiotic treatment, evacuation should be emergent.11 Dacryocystitis is an infection of the lacrimal sac that typically arises from obstruction of the lacrimal duct, which causes pooling of tears in the lacrimal sac and subsequent infection.4 It presents as pain, swelling, and redness over the lacrimal duct, which is located at the nasal corner of the eye. The most common pathogens involved areS aureus, Streptococcus species, and H influenzae.12 Dacrocystitis can be treated initially with oral antibiotics as well as warm compresses, if available. The preferred antibiotic is amoxicillin/clavulanate 875 mg orally, 2 times daily for 10 days, but if that is not included in your kit, oral fluoroquinolones (such as moxifloxacin) will likely suffice.10 If this condition worsens, the patient should be evacuated, nonemergently.

  • Antibiotics:1C
  • Emergent evacuation for orbital cellulitis:1C
  • Nonemergent evacuation for periorbital cellulitis:1C

ACUTE RED EYE

There are numerous conditions that can cause redness of the eye, and the severity of these conditions can range from mild to severe. There are 3 main tests that can be quickly and easily accomplished to help make the diagnosis:fluorescein staining, relief of pain with anesthetic drops, and pupillary status.11 These tests can be easily performed in the wilderness if the supplies are available. The medical causes of the red eye can be broadly divided into conditions that are fluorescein positive (corneal ulcer or erosion, herpes keratitis), and those that are negative. Those that are negative can be further divided into conditions that resolve with an initial dose of topical anesthetic (conjunctivitis, blepharitis, ultra- violet [UV] keratitis) and those that do not (acute angle- closure glaucoma [AACG], iritis, scleritis).

ACUTE ANGLE-CLOSURE GLAUCOMA

Acute angle-closure glaucoma is caused by a blockage of aqueous outflow from the eye resulting in increased intraocular pressure (IOP). Symptoms include deep and severe pain, blurry vision, halos around lights, headache, and often nausea and vomiting.13 Signs of this diagnosis include a nonreactive pupil that is mid dilated (4 mm to 6 mm), decreased visual acuity, “steamy” or “hazy” cornea, and a red eye.14 Measurement of IOP in the field is often impossible owing to the absence of measurement devices, but gentle palpation of the globe through a closed lid may reveal a taut globe indicating elevated IOP.13,15,16 The palpation should be done very gently and also in comparison with the normal eye. AACG is a medical emergency and requires emergent evacuation, as the definitive treatment is surgical. Standard treatment of AACG includes timolol 0.5%, 1 drop in the affected eye 2 times daily, topical steroids such as prednisolone 1%, 1 drop 4 times daily, and oral acetazolamide (Diamox), 500 mg 2 times daily.4,17 Pilocarpine 1% to 2%, 1 drop every 15 minutes for 2 doses should be given 1 hour after other treatments have been given. Additionally, patients should be advised to lie flat for at least 1 hour.17

  • Medical management:1B
  • Surgical management:1A
  • Emergent evacuation:1C

IRITIS

Nontraumatic iritis (also called anterior uveitis) is inflammation of the iris that is inflammatory or infectious. Many symptoms are similar to previously noted conditions including pain, redness of the conjunctiva, blurred vision, and photophobia. The patient may also have a history of iritis, which is a good clue to the diagnosis. One important examination finding is photophobia with shining of a penlight in the unaffected eye (consensual photophobia).14 Standard therapy for iritis includes corticosteroids, such as prednisolone 1% eye drops, 1 drop into the affected eye every hour if severe, every 4 hours if mild.18 If drops are unavailable, or if the condition is worsening, oral steroids can be given, prednisone 40 mg to 60 mg oral daily. If there is concern for herpetic lesions or other serious infection, steroids should be avoided. In this case, a topical nonsteroidal anti-inflammatory drug (NSAID) may be beneficial. Cycloplegic (mydriatic) drops, such as atropine, are a key component to pain control as they relieve ciliary spasm.18 Place 1 drop in the affected eye 2 times daily. Evacuation should be emergent, as iritis can be complicated by scarring of the pupil and elevated IOP, leading to decreased vision or blindness.11

  • Topical steroids:1C
  • Systemic steroids:2C
  • Mydriatic drops:1C
  • Topical NSAID: 2C
  • Emergent evacuation:1C

HERPES KERATITIS

Herpes keratitis is diagnosed by a dendritic staining pattern on fluorescein examination. Often, patients have had previous episodes of ocular herpes infections.13 Treatment includes oral or ophthalmic preparations of trifluridine or acyclovir, although these are often not included in expedition kits.19 Participants should be encouraged to bring their own medicine if they have a history of this condition. Steroids should be avoided for patients with suspected herpes keratitis.20 Although some texts advocate debridement of herpetic lesions with a cotton-tipped swab, that has not been proven to be efficacious and should only be done by experienced providers if deemed necessary.19

  • Oral or ophthalmic antivirals:1A

CONJUNCTIVITIS

Among fluorescein-negative medical eye conditions, conjunctivitis, blepharitis, and UV keratitis can usually be treated in the field, and are typically not serious. Conjunctivitis is the most common cause of a red eye.13 Common etiologies include allergies, viruses, and bacteria. Conjunctivitis always involves the palpebral conjunctiva, and the examiner must look under the lid to evaluate for this inflammation. The hallmark of allergic conjunctivitis is itching. Bacterial conjunctivitis gives a purulent discharge, whereas viral conjunctivitis tends to give a watery discharge. Treatment of allergic and viral conjunctivitis is primarily supportive, and bacterial conjunctivitis is treated with antibiotics. Although bacterial conjunctivitis is usually a self-resolving condition, studies have demonstrated that use of antibiotics results in faster clinical and microbiological remission.21 There are no studies showing superiority of any one antibiotic over another; therefore, choice should be based on availability.22 Erythromycin ointment, a 1-cm ribbon placed in the lower conjunctival sac 3 or 4 times daily for 7 days, is a reasonable option. It is important to note that viral conjunctivitis is extremely contagious, and proper hand washing is essential in wilderness settings to avoid spread throughout a group or to the contralateral eye.23 Topical anesthetic eye drops are diagnostically beneficial and provide acute relief for corneal ulcers, herpes keratitis, and conjunctivitis; however, it is important to note that they should not be used chronically as they are toxic to the corneal epithelium.23

  • Topical or systemic antibiotics:1A
  • Hand washing:1C

Altitude and the Eye

The environmental conditions at altitude, including hypoxia and low atmospheric pressure, pose several problems for the eye and may result in problems both for the previously healthy eye and for the patient with a history of ocular disease. Because the cornea receives most of its oxygen from the ambient air, the cornea becomes hypoxic at altitude and may not function normally.24 In addition, patients with a history of intraocular gas bubbles should not go to high altitude owing to expansion of the gas bubble at decreasing atmospheric pressure. Patients should consult with their ophthalmologist regarding the safety of traveling to altitude.

ALTITUDE AFTER RADIAL KERATOTOMY, LASER-ASSISTED STROMAL IN SITU KERATOMILEUSIS, OR PHOTOREFRACTIVE KERATOTOMY

Hypoxia at altitude causes edema and thickening of the cornea.25,26 Although this thickening has been shown not to cause visual disturbances in healthy eyes, it can be problematic for patients who have undergone radial keratotomy (RK), laser-assisted stromal in situ keratomileusis (LASIK), or photorefractive keratotomy (PRK). Radial keratotomy involves making incisions into the cornea, weakening its stability. The edema caused by the hypoxia of high altitude results in a flattening of these corneas, causing increased far-sightedness24 and a significant decrease in visual acuity. The amount of vision change partially depends on the amount of residual myopia that a patient has at sea level, but is difficult to predict before altitude exposure. Although most of these changes will resolve with return to normal altitude, it is recommended that patients who have had RK take various levels of corrective lenses during their excursion. The cheapest option may be to wear glasses under goggles and to bring several levels of corrective glasses. The best option, however, would be to bring several levels of prescription goggles in the event of decreased visual acuity at altitude. Patients should consult with their ophthalmologist to obtain various strengths of eyewear. Eyes that have received LASIK and PRK undergo fewer refractive changes at altitude. There have been 2 studies demonstrating blurring of vision at altitude, and 2 studies demonstrating no change. A recent study of 12 climbers with LASIK-treated eyes noted no visual changes with changing altitude, despite dry eye associated with high altitude mountaineering being a known complication of LASIK.27 Similarly, post-PRK patients seem to have excellent vision at altitude. There has only been 1 study of this PRK population, and it demonstrated no significant change in vision at altitude.28

  • Caution at high altitude if history of RK:1C
  • Safety of LASIK/PRK at altitude:1C
  • Extra goggles/glasses if history of RK:1C

HIGH-ALTITUDE RETINAL HEMORRHAGE

At altitude an increase in retinal blood flow and subsequent retinal vein dilation11 can lead to retinal hemorrhages, which have been well described since the 1970s.29 The percentage of climbers experiencing retinal hemorrhages ranges from 4% to 82%, depending on the study.29 Most cases of retinal hemorrhage do not cause visual disturbances, unless the hemorrhage involves the macula. Patients with retinal hemorrhages can continue ascent if no visual disturbances are present, but should be instructed to descend in the setting of altered vision.11 Additionally, the presence of high altitude retinal hemorrhage has been associated with altitude illness, and its presence should alert providers to the possible development of altitude illness.

  • Descent if visual changes:1C

Diving and the Eye

The hyperbaric environment can cause a number of effects on the eye. The primary concerns regarding dive medicine and the eye include ensuring that patients have normal visual acuity while diving, and making sure that patients who have a surgical intraocular gas bubble do not dive. Divers who normally require corrective lenses should dive with prescription goggles or soft contact lenses. Diving after refractive surgery such as LASIK and PRK is safe.30 Diving after RK carries a hypothetical risk of corneal incision rupture, although in practice this is not seen, and diving is therefore considered safe. Additionally, divers who have had RK cannot dive for 6 months postoperatively to ensure adequate wound healing of the corneal incisions. Divers with a history of any type of eye surgery should always consult with their ophthalmologist before diving.31

  • Safety of diving after refractive surgery:1C

OCULAR AND PERIOCULAR BAROTRAUMA

A complete description of the mechanism and pathophysiology of barotrauma are beyond the scope of this review; however, in brief, when air in a closed space is exposed to higher atmospheres of pressure, it is compressed. If this occurs while diving with a facemask, the lids, skin, and eyes can be drawn out into the mask. This force can be very strong and cause significant injury, resulting in periorbital ecchymosis, edema, subconjunctival hemorrhage, and potentially hyphema. The prevention of ocular and periocular barotrauma can be achieved by frequently filling one’s mask with exhaled air from the nose to increase the volume of air in the mask.31–33

  • Mask pressure equalization:1C

Traumatic Eye Injuries

The treatment of traumatic ocular emergencies in the wilderness hinges on rapid assessment, stabilization, and evacuation. Often eye injuries do not occur in isolation and may be associated with other potentially life- threatening injuries. Periocular and ocular traumas include many disorders, but these guidelines are limited to the most commonly encountered conditions in the wilderness. Ocular trauma is responsible for approximately 3% of emergency department visits in North America annually34 and is a leading cause of preventable blindness worldwide. Its true incidence in the wilderness is unknown as epidemiologic data are absent from the literature.

PERIOCULAR TRAUMA

Eyelid lacerations

Falls, branches, rocks, or animal bites can cause eyelid lacerations. Eyelid lacerations can be classified as simple or complex. Simple lid lacerations are often horizontal and partial thickness, and do not involve the lid margin. This type of laceration can be managed with irrigation and typical wound care and has an excellent prognosis.35 Eyelid lacerations that are complex, namely, full thickness, and involve the lid margin or the medial or lateral end of the palpebral fissures require evacuation and emergent ophthalmologic evaluation and repair, ideally within 36 hours.35,36 Immediate treatment consists of prompt irrigation and the application of antibiotic ointment with shielding to protect the eye as evacuation commences. If an associated ruptured globe is suspected, there should be no further examination, manipulation, or irrigation of the eye. Treatment should be as outlined in the section on ruptured globe.

  • Wound care:1B
  • Antibiotic ointment:1B
  • Eye shield:1C
  • Emergent evacuation if complex eyelid laceration:1B

Orbital fractures

A direct blow to the face or orbit may cause fractures of any of the 7 facial bones that form the orbit. Orbital fractures can lead to significant ocular injury and subsequent visual impairment in approximately 17% of cases.37 Thus, it is important for the wilderness provider to be able to perform a basic ophthalmologic examination to screen for severe injury, including entrapment of ocular muscles and pupillary or vision derangements. If signs of entrapment or visual derangements are present, emergent evacuation is required. Clinically significant retro-orbital hemorrhage can cause a compressive optic neuropathy and is a true ophthalmologic emergency. Signs include markedly elevated IOP, vision loss, and an afferent pupillary defect. If it is within the wilderness practitioner’s scope of training and practice, an emergent lateral cantholysis and canthotomy may restore vision in patients with compressive optic neuropathy attributable to retro- orbital hemorrhage. Therefore, emergent, expert management both in the field (with a cantholysis/canthotomy procedure, if indicated) and during emergent evacuation to the closest emergency center are essential. As a result of consensus review in both maxillofacial and ophthalmologic practice patterns, patients with suspected orbital fractures should avoid blowing their nose until cleared to do so by a specialist. Patients may find relief from congestion through the use of nasal decongestant sprays, and if systemic steroids are available, they may be used to decrease orbital edema.38,39 Beyond this basic medical management, emergent evacuation is imperative if signs of ocular muscle entrapment, traumatic vision loss, or suspected globe rupture are present.

  • Orbital fractures
  • Nose blowing:1C
  • Decongestant sprays:1C
  • Systemic steroids:2C
  • With entrapment or visual derangements, emergent evacuation:1B
  • Retro-orbital hemorrhage
  • Lateral cantholysis:1B
  • Emergent evacuation:1B

OCULAR TRAUMA

Globe rupture

Globe rupture or an open globe results from trauma and is an ophthalmologic emergency that requires emergent evacuation from the wilderness. A soft eye often characterizes an open globe, although palpation of the eye must be avoided in globe rupture as it may cause progression of the injury. If the anterior segment is involved in the rupture, the iris may prolapse into the wound, causing an irregular or a keyhole-shaped pupil. Such a change in pupil shape is extremely suggestive of a serious anterior segment injury that is in need of emergent evacuation for an ophthalmology consultation. The complications of globe rupture are endophthalmitis, defined as infection and inflammation of the contents of the globe, or potential vision loss, or both. In one review, lacerations of the globe that failed to self-seal and did not have intraocular tissue prolapse were at higher risk for development of endophthalmitis.40 It has also been shown that primary repair more than 24 hours from injury is an independent risk factor in developing endophthalmitis.40 Treatment of endophthalmitis generally requires antibiotics and corticosteroids that can be administered by a variety of routes.40 Because of the likelihood of contamination after globe rupture in the wilderness setting, a strong pathophysiologic rationale exists for the early administration of broad-spectrum antibiotics, if available, that will cover Clostridium species,S aureus, Streptococcus species, and Pseudomonas species. The selected antibiotic must also have good eye penetration, which makes moxifloxacin, 400 mg orally once daily, a good antibiotic choice. Topical antibiotics should be avoided. In the wilderness, the patient’s eye should be shielded to avoid further injury. A pressure patch should not be used as it can result in the expulsion of the intraocular contents. All foreign bodies, if large enough to be visualized, should be left in place and splinted with a shield until evaluated by a specialist.41

  • Shielding:1C
  • Early antibiotics:1B
  • Steroids:1B
  • Emergent evacuation:1A

Hyphema

A hyphema is a collection of blood in the anterior chamber between the iris and the cornea, generally after trauma. The collection of blood is usually an isolated finding, but can accompany a dislocated lens, ruptured globe, or retinal injury. The majority of hyphemas resolve without treatment, but patients need to be monitored for secondary complications including corneal staining, rebleeding, and acute elevation in IOP. Therefore, this condition in the wilderness requires emergent evacuation.42 There is no difference between ambulation and complete rest on the risk of secondary hemorrhage or time to rebleeding.42 Despite this report, in the wilderness, based on the current pathophysiologic understanding of hemostasis, activity should be restricted to walking only. Available evidence regarding the use of cycloplegics or corticosteroids in traumatic hyphema is lacking.42 Historically, cycloplegics (atropine 1%, every 8 hours) and topical corticosteroids (prednisolone acetate 1%, 4 times a day) have been used to decrease inflammation and improve a patient’s comfort, and should be considered for this purpose.42 If clinical signs of increased IOP are present, such as headache, nausea, or vomiting, or if the affected globe is taut under palpation in comparison with the unaffected eye, then addition of topical or systemic IOP-lowering medications are indicated.15 In the wilderness setting, acetazolamide may be available and can be used for this purpose at a dose of 500 mg orally twice daily.43 Analgesics and antiemetics should be used as clinically indicated to keep the patient comfortable and to minimize emesis, which can elevate IOP and worsen bleeding.15,42,44 Patient positioning should keep the head elevated above 30 degrees at all times. There is no difference between a single patch versus a binocular patch on the risk of secondary hemorrhage or time to rebleeding.42 Given the risk of rebleeding, NSAIDs should be avoided.44 Although no direct evidence is available, near work or tasks (eg, reading) are also not recommended as the accommodation reflex moves the iris and can worsen rebleeding. A rigid shield is not effective in preventing rebleeding, but may be used to prevent further trauma.42 If a hyphema is found, emergent evacuation for expert consultation is recommended.

  • Activity restriction:1C
  • Corticosteroids or cycloplegics:1C
  • IOP-lowering medications:1A
  • Acetazolamide:1B
  • Analgesics and antiemetics:1C
  • Use of a rigid shield:1B
  • Avoidance of NSAIDs:1B
  • Emergent evacuation:1B

Corneal abrasion

Corneal abrasions are one of the most frequently encountered ocular conditions and are most commonly caused by a foreign body, a direct blow to the eye, or the use of contact lenses. If a corneal foreign body is evident, then prompt removal is recommended. It is important to consider open globe injury with any corneal trauma. If open globe is suspected or deep corneal epithelial defects are apparent, then evacuation is emergent. Corneal abrasions should be treated with topical antibiotics (such as erythromycin ophthalmic 0.5% ointment, 1 cm every 8 hours),45,46 cycloplegics (such as atropine 1%, 1 drop every 8 hours),46 NSAIDs (such as ketorolac 0.5%, 1 drop every 8 hours),47 and frequent use of artificial tears.46 Sunglasses may help reduce photophobia, but there is no evidence to support eye patching for corneal abrasions. Bandage soft contact lenses can provide significant relief, restore depth perception, and improve function, but should be used only if 1) there is no retained corneal foreign body; 2) they are used in conjunction with a prophylactic topical antibiotic drop; and 3) they are removed within 24 to 48 hours. Topical anesthetic eye drops are diagnostically beneficial and provide acute relief for corneal abrasions and ulcers—but it is important to note that they should not be used chronically as they are potentially toxic to the corneal epithelium.18 Despite this axiom, a recent prospective, double-blind, randomized trial of tetracaine versus saline for the treatment of uncomplicated corneal abrasions concluded that there was no significant difference in corneal healing and an overall patient perception of improved pain control.48

  • Topical antibiotics:1A
  • Cycloplegics:1A
  • NSAIDs:1A
  • Artificial tears:1C
  • Sunglasses:1C
  • Avoidance of patching:1A
  • Emergent evacuation for open globe or deep epithelial defects:1C

Corneal ulcers

Corneal ulceration differs from abrasion in that the cause of acute ulceration is often infectious. Additionally, whereas a corneal abrasion is damage to the surface epithelial tissue of the cornea, ulceration involves deeper layers of the cornea. Signs include significant pain in the eye, white or gray infiltrate on the cornea on penlight evaluation, and an epithelial defect on fluorescein examination.11 Risk factors for ulceration include previous corneal abrasion as well as contact lens wear, particularly with improper care of contact lenses or continued use for prolonged periods. Emergent treatment is important, as ulcers can enlarge, causing decreased visual acuity and corneal scarring or perforation. If a corneal ulcer is present, contact lenses must be discontinued.

If the patient is within 4 hours of an ophthalmologist’s evaluation, it is preferable that the ophthalmologist obtains a culture before initiating treatment. If the patient is more than 4 hours from an expert evaluation, then empiric treatment should begin. Empiric treatment includes fourth-generation fluoroquinolone eye drops, such as moxifloxacin 0.5%. The patient should be loaded with the drops by instilling 1 drop every 5 minutes for the first 30 minutes, then 1 drop every 30 minutes for 6 hours, followed by 1 drop every hour until the patient is able to see an ophthalmologist.49,50 Oral Fluoroquinolones are warranted for wilderness cases if nothing else is available (such as moxifloxacin, 400 mg daily for 7 days). Cycloplegic medication (such as atropine 1%, 1 drop every 8 hours) can also be given to prevent synechiae formation and decrease pain in severe cases. Evacuation should be emergent.11

  • Antibiotics, topical:1B
  • Antibiotics, systemic:1C
  • Cycloplegic:1B
  • Emergent evacuation:1C

Chemical eye injuries

Chemical eye injuries in the wilderness are limited to case reports and case series, the most robust of which is related to the spitting cobra (genus Naja), primarily found in Africa. Other chemical injuries have been incurred through skunk musking, jellyfish stings, and exploding or spraying of cooking gases. The spitting cobra can eject its venom several meters into the eyes of its victim.51 The venom can cause severe chemosis, blepharitis, and corneal irritation. Opacification with corneal and subconjunctival neovascularization (termed the“corneal opacification syndrome”)often leads to blindness and is most often associated with the black cobra (Naja nigricollis).52,53 There is some evidence from rabbit studies that tetracycline drops and systemic heparin have a protective effect in guarding against corneal opacification syndrome.52 Currently, there is no indication for topical or intravenous antivenom administration.54 Prevention of chemical injuries is the most important tenet in this category, as treatment in the wilderness is largely supportive for such injuries. In general, rapid, large- volume irrigation and analgesia are the mainstays of treatment.54 Ultimately, after chemical eye injury, emergent evacuation and expert consultation are encouraged.54

  • Large-volume irrigation:1C
  • Topical antibiotics:1C
  • Evacuation:1C
  • Animal-related bites and envenomations—systemic and topical antibiotics:1C
  • Emergent evacuation:1C

Ultraviolet keratitis

Ultraviolet keratitis is a self-limited, inflammatory disorder of the cornea caused by UV rays. Symptoms of severe pain, burning, and tearing with a red eye, 6 to 12 hours after exposure to UV rays, should raise the suspicion of this condition. Although no prospective studies have looked at treatment of UV keratitis specifically, treatment is similar to that for corneal abrasions. That includes topical antibiotic ointments, anti-inflammatory drugs, and cycloplegics. (See previous section regarding dosing.) Artificial tears and patching are not recommended. Systemic analgesia is also recommended if severe pain is present. Evacuation should commence in a nonemergent manner if treatment is not available in the wilderness setting. Prevention is the mainstay of treatment, with adequate sunglasses with side-shields being the most important mechanism for prevention.55

  • Sunglasses:1C
  • Topical antibiotics:1C
  • Cycloplegics:1C
  • NSAIDs:1C
  • Artificial tears:1C
  • Nonemergent evacuation:1C

Corneal frostbite

Corneal frostbite has been described only in case reports and book passages. Its treatment would follow similar guidelines as for other corneal epithelial disorders, including those listed under treatment for UV keratitis.56–58

  • Topical antibiotics:1C
  • Cycloplegics:1C
  • NSAIDs:1C
  • Artificial tears:1C

Traumatic iritis

Traumatic iritis is acute inflammation of the anterior uveal tract that can occur after trauma. In the wilderness, the diagnosis is made from a history of pain and photophobia that is often consensual. Inflammation can occur in the absence of visible ocular trauma.14 This condition is often self-limited, and topical steroids (such as prednisolone acetate 1%, 1 drop every 2 hours when awake for the first week and then tapered slowly) and NSAIDs (such as ketorolac 0.5%, 1 drop every 8 hours)59 can reduce inflammation, whereas cycloplegics (such as atropine 1%, 1 drop every 8 hours) can make the patient more comfortable until the inflammation is resolved.60 Evacuation should commence in a nonemergent manner if treatment is not available in the wilderness setting.

  • NSAIDs:1B
  • Oral steroids:1B
  • Topical steroids:1B
  • Cycloplegics:1B
  • Nonemergent evacuation:1C

Subconjunctival hemorrhage

Bleeding between the conjunctiva and sclera causes a collection of blood that appears bright red. Although impressive looking, this condition will resolve in days to weeks without treatment.60 Unless there are signs of a ruptured globe or basilar skull fracture, no backcountry treatment or evacuation is required.

Conclusions

Wilderness eye injuries encompass a diverse group of illnesses that often require specialized equipment, medications, and expertise. This review provides an evidence-based overview of the most commonly encountered eye injuries; however, evidence regarding wilder- ness treatment is limited to case reports and the extrapolation of clinical and hospital care. Treatment in the wilderness is often based on available supplies and treatments rather than on the most evidence-based interventions. However, with the proper tools and physical examination skills, most providers can determine the need for further intervention or evacuation in cases of ocular pathology in the wilderness.

Supplementary tables

Supplementary ACCP Table 1 and Evidence Table 2 are available online at http://dx.doi.org/10.1016/j.wem.2014.08.008.

References

  1. Cohn MJ, Kurtz D. Frequency of certain urgent eye problems in an emergency room in Massachusetts.JAm Optom Assoc. 1992;63:628– 633.
  2. Forgey W.Wilderness Medical Society: Practice Guidelines for Wilderness Emergency Care.Guilford, CT: Globe Pequot Press; 2001.
  3. Guyatt G, Gutterman D, Baumann MH, et al. Grading strength of recommendations and quality of evidence in clinical guidelines: report from an American College of Chest Physicians Task Force.Chest. 2006;129:174– 181.
  4. Marx J, Hockberger R, Walls R. Rosen’s Emergency Medicine. 7th ed. Philadelphia, PA: Mosby; 2010.
  5. Butler FK Jr, Hagan C, Murphy-Lavoie H. Hyperbaric oxygen therapy and the eye. Undersea Hyperb Med. 2008;35:333– 387.
  6. Fraser SG, Adams W. Interventions for acute non-arteritic central retinal artery occlusion.Cochrane Database Syst Rev. 2009(1):CD001989.
  7. Kiire CA, Chong NV. Managing retinal vein occlusion. BMJ. 2012;344:e499.
  8. Howe L, Jones NS. Guidelines for the management of periorbital cellulitis/abscess.Clin Otolaryngol Allied Sci. 2004;29:725– 728.
  9. Baring DE, Hilmi OJ. An evidence based review of periorbital cellulitis.Clin Otolaryngol. 2011;36:57– 64.
  10. Pinar-Sueiro S, Sota M, Lerchundi TX, et al. Dacryocystitis: systematic approach to diagnosis and therapy.Curr Infect Dis Rep. 2012;14:137– 146.
  11. Butler F. The eye in the wilderness. In: Auerbach PS, ed. Wilderness Medicine.6th ed. St. Louis, MO: Mosby; 2011.
  12. Mandell GL, Bennett JE, Dolin R.Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases. 7th ed. Philadelphia, PA: Churchill Livingstone/Elsevier; 2010.
  13. Mahmood AR, Narang AT. Diagnosis and management of the acute red eye.Emerg Med Clin North Am. 2008;26: 35 – 55, vi.
  14. Dargin JM, Lowenstein RA. The painful eye.Emerg Med Clin North Am. 2008;26:199–216, viii.
  15. Brandt MT, Haug RH. Traumatic hyphema: a comprehensive review.J Oral Maxillofac Surg. 2001;59:1462– 1470.
  16. Baum J, Chaturvedi N, Netland PA, Dreyer EB. Assessment of intraocular pressure by palpation.Am J Ophthalmol. 1995;119:650– 651.
  17. Choong YF, Irfan S, Menage MJ. Acute angle closure glaucoma: an evaluation of a protocol for acute treatment. Eye (Lond). 1999;13:613– 616.
  18. Wilson SA, Last A. Management of corneal abrasions.Am Fam Physician. 2004;70:123– 128.
  19. Wilhelmus KR. Antiviral treatment and other therapeutic interventions for herpes simplex virus epithelial keratitis. Cochrane Database Syst Rev. 2010(12):CD002898.
  20. Morrow GL, Abbott RL. Conjunctivitis.Am Fam Physician. 1998;57:735– 746.
  21. Sheikh A, Hurwitz B. Antibiotics versus placebo for acute bacterial conjunctivitis. Cochrane Database Syst Rev. 2006;(2):CD001211. Updated 2012.
  22. Høvding G. Acute bacterial conjunctivitis.Acta Ophthalmol. 2008;86:5– 17.
  23. Rapuano CJ.American Academy of Ophthalmology Cornea/External Disease Panel. Preferred Practice Pattern Guidelines. Conjunctivitis.San Francisco, CA: American Academy of Ophthalmology; 2008.
  24. Mader TH, Tabin G. Going to high altitude with preexisting ocular conditions.High Alt Med Biol. 2003;4:419– 430.
  25. Bosch MM, Barthelmes D, Merz TM, et al. New insights into changes in corneal thickness in healthy mountaineers during a very-high-altitude climb to Mount Muztagh Ata. Arch Ophthalmol. 2010;128:184– 189.
  26. Morris DS, Somner JE, Scott KM, McCormick IJ, Aspinall P, Dhillon B. Corneal thickness at high altitude.Cornea. 2007;26:308– 311.
  27. Dimmig JW, Tabin G. The ascent of Mount Everest following laser in situ keratomileusis. J Refract Surg. 2003;19:48– 51.
  28. Mader TH, Blanton CL, Gilbert BN, et al. Refractive changes during 72-hour exposure to high altitude after refractive surgery.Ophthalmology. 1996;103:1188– 1195.
  29. Hackett PH, Rennie D. Rales, peripheral edema, retinal hemorrhage and acute mountain sickness. Am J Med. 1979;67:214– 218.
  30. Huang ET, Twa MD, Schanzlin DJ, Van Hoesen KB, Hill M, Langdorf MI. Refractive change in response to acute hyperbaric stress in refractive surgery patients.J Cataract Refract Surg. 2002;28:1575– 1580.
  31. Butler FK Jr. Diving and hyperbaric ophthalmology.Surv Ophthalmol. 1995;39:347– 366.
  32. Butler FK, Gurney N. Orbital hemorrhage following face- mask barotrauma.Undersea Hyperb Med. 2001;28:31– 34.
  33. Butler FK, Bove AA. Infraorbital hypesthesia after maxillary sinus barotrauma.Undersea Hyperb Med. 1999;26: 257 – 259.
  34. Bord SP, Linden J. Trauma to the globe and orbit.Emerg Med Clin North Am. 2008;26:97–123, vi-vii.
  35. Chang EL, Rubin PA. Management of complex eyelid lacerations.Int Ophthalmol Clin. 2002;42:187– 201.
  36. Murchison AP, Bilyk JR. Management of eyelid injuries. Facial Plast Surg. 2010;26:464– 481.
  37. Brown MS, Ky W, Lisman RD. Concomitant ocular injuries with orbital fractures.J Craniomaxillofac Trauma. 1999;5:41– 48.
  38. Lelli GJ Jr, Milite J, Maher E. Orbital Floor fractures: evaluation, indications, approach, and pearls from an ophthalmologist’s perspective.Facial Plast Surg. 2007; 23:190– 199.
  39. Joseph JM, Glavas IP. Orbital fractures: a review.Clin Ophthalmol. 2011;5:95– 100.
  40. Zhang Y, Zhang MN, Jiang CH, Yao Y, Zhang K. Endophthalmitis following open globe injury.Br J Ophthalmol. 2010;94:111– 114.
  41. Pokhrel PK, Loftus SA. Ocular emergencies.Am Fam Physician. 2007;76:829– 836. 42.Gharaibeh A, Savage HI, Scherer RW, Goldberg MF, Lindsley K. Medical interventions for traumatic hyphema. Cochrane Database Syst Rev. 2011;1:CD005431. Updated 2013.
  42. FDA. Diamox. 2012. Available at: http://www.drugs.com/pro/diamox.html. Accessed March 5, 2012.
  43. Walton W, Von Hagen S, Grigorian R, Zarbin M.Management of traumatic hyphema. Surv Ophthalmol.2002;47:297– 334.
  44. Upadhyay MP, Karmacharya PC, Koirala S, et al. The Bhaktapur eye study: ocular trauma and antibiotic prophylaxis for the prevention of corneal ulceration in Nepal.Br J Ophthalmol. 2001;85:388– 392.
  45. Fraser S. Corneal abrasion.Clin Ophthalmol. 2010;4:387–390.
  46. Weaver CS, Terrell KM. Evidence-based emergency medicine. Update: do ophthalmic nonsteroidal anti-inflammatory drugs reduce the pain associated with simple corneal abrasion without delaying healing? Ann Emerg Med. 2003;41:134– 140.
  47. Waldman N, Densie IK, Herbison P. Topical tetracaine used for 24 hours is safe and rated highly effective by patients for the treatment of pain caused by corneal abrasions: a double-blind, randomized clinical trial.Acad Emerg Med. 2014;21:3784– 3782.
  48. American Academy of Ophthalmology Cornea/External Disease Panel, Preferred Practice Pattern Guidelines, Bacterial Keratitis-Limited Revision.San Francisco, CA: American Academy of Ophthalmology; 2011.
  49. Shah VM, Tandon R, Satpathy G, et al. Randomized clinical study for comparative evaluation of fourth- generation fluoroquinolones with the combination of fortified antibiotics in the treatment of bacterial corneal ulcers.Cornea. 2010;29:751– 757.
  50. Grüntzig J. Spitting cobra ophthalmia (Naja nigricollis) [in German].Klin Monatsbl Augenheilkd. 1984;185:527– 530.
  51. Ismail M, al-Bekairi AM, el-Bedaiwy AM, Abd-el Salam MA. The ocular effects of spitting cobras: I. The ringhals cobra (Hemachatus haemachatus) venom-induced corneal opacification syndrome.J Toxicol Clin Toxicol. 1993;31:31– 41.
  52. Ismail M, al-Bekairi AM, el-Bedaiwy AM, Abd-el Salam MA. The ocular effects of spitting cobras: II. Evidence that cardiotoxins are responsible for the corneal opacification syndrome.J Toxicol Clin Toxicol. 1993;31:45– 62.
  53. Chu ER, Weinstein SA, White J, Warrell DA. Venom ophthalmia caused by venoms of spitting elapid and other snakes: report of ten cases with review of epidemiology, clinical features, pathophysiology and management.Toxicon. 2010;56:259– 272.
  54. McIntosh SE, Guercio B, Tabin GC, Leemon D, Schimelpfenig T. Ultraviolet keratitis among mountaineers and outdoor recreationalists.Wilderness Environ Med. 2011; 22:144– 147.
  55. Lantukh VV. Effect of northern climate on the eye [in Russian].Vestn Oftalmol. 1983;1:58– 61. 57.Korablev AF. Case of transitory keratopathy in a skier caused by low air temperature and maximal physical exertions [in Russian].Vestn Oftalmol. 1981;2:72.
  56. Forsius H. Climatic changes in the eyes of Eskimos, Lapps and Cheremisses.Acta Ophthalmol (Copenh). 1972;50: 532 – 538.
  57. Kempen JH, Altaweel MM, Holbrook JT, et al. Multicenter Uveitis Steroid Treatment (MUST) Trial Research Group. Randomized comparison of systemic antiinflammatory therapy versus fluocinolone acetonide implant for intermediate, posterior, and panuveitis: The Multicenter Uveitis Steroid Treatment Trial.Ophthalmology. 2011;118:1916– 1926.
  58. Cronau H, Kankanala RR, Mauger T. Diagnosis and management of red eye in primary care. Am Fam Physician. 2010;81:137– 144.