EMERGENCY MANAGEMENT

Treating polytraumatized patients can be extremely challenging, requiring rapid and efficient collaboration of multiple specialists and paramedical personnel

(e.g., nurses, technicians, emergency physicians, surgeons, radiologists, anesthesiologists, operating room personnel, even interpreters).

PEARL... Emergency medical technicians, police, and fire fighters often provide critical details of the injury and past medical

history. They also help to preserve the integrity of evidence that might later be used in court.

In the initial phase of emergency medical care, the visual system commonly has low priority, but loss of vision can significantly diminish the quality of life for the otherwise rehabilitated patient and may result in the most devastating long-term disability.1

EPIDEMIOLOGY

A retrospective analysis1 of 1119 cases from a major hospital over a 7-year period (Fig. 10–1) found the following:

•age ranged from 15 to 90 years;

•80% of the patients were male;

•16% suffered ocular or adnexal injuries and 23% of these patients died;

•29% had facial injuries, of which 55% were ocular injuries; and

•1.2% of injuries resulted in vision less than 20/200.

Significant eye injury was statistically associated with the following:

•driving a motor vehicle;

•age younger than 50 years;

•male sex;

•associated basal skull fracture;

•orbital fracture; and

•lid laceration or superficial eye injury.

Of the patients with the most severe injuries:

•0.8% had open globe injuries;

•1.9% had optic nerve trauma, half of whom had vision less than 20/200; and

•9.2% had orbital fracture.

In another study, among 6313 patients with major injuries admitted to a level I trauma facility over a 4-year period, 14% were found to have concomitant eye injury, most commonly eye/adnexa contusion (67%), adnexal lacerations (27%), and open globe injury (4%).2

INITIAL ASSESSMENT

The initial steps are based on the general principles of advanced trauma life support.a

a Ensuring the patency of the airway and establishing breathing and cardiovascular stability (ABC).

PEARL... In many cases, it is helpful for the ophthalmologist to be present in the ER or trauma room to try to protect the

eyes during manipulations of the mouth, nose, and trachea. Emergency ocular problems (e.g., chemical burn, central retinal artery occlusion, open globes, retrobulbar hemorrhage) must also be addressed early.

PEARL... In patients with severe intracranial injuries in whom changes in pupil size and reactivity may presage impend-

ing herniation and the need for immediate neurosurgical intervention, the integrity of the pupil (i.e., no pharmacologic dilation) is more important than the information provided by dilated-pupil IBO.

When possible, an initial assessment of the vision should be performed, although altered mental status as a result of intracranial trauma or the use of analgesia or anesthesia may prevent this. The miotic effect of narcotic agents can hinder the examination of the pupils and the retina.

Finally, urgent ophthalmic problems should be assessed; in most cases, the initial triage is possible using only a penlight examination. The eye’s repair often has to be coordinated with other surgical interventions (e.g., an open globe should be closed before orbital surgery is performed; see Chapter 12).

EMERGENCY INTERVENTION

Ocular conditions requiring immediate evaluation and/or intervention include:

•chemical burn (see Chapter 11) and, to a lesser extent,

•retrobulbar hemorrhage (see Chapter 12) and

•open globe injury (see Chapter 9).

OPEN GLOBE INJURY AND THE

NONOPHTHALMOLOGIST

Signs that suggest the presence or possibility of open globe trauma include:

•obvious open wound;

•collapsed or severely distorted eye;

•prolapsed uveal tissue;

•peaked pupil;

•subconjunctival hemorrhage with shallowing or deepening of the AC; and/or

•ocular hypotony with or without subconjunctival hemorrhage.

RADIOLOGIC EVALUATION

The eyes, orbits, and surrounding bones are best visualized with a noncontrast CT scan, which can usually be obtained concurrently with the imaging of the brain, thorax, and abdomen typically necessary in the evaluation of these patients (see Chapter 9).

SPECIAL CONSIDERATIONS

Children

In children with polytrauma, there are unique legal implications because of abuse. Abuse annually involves approximately 900,000 children in the United States3 (see also Chapters 9, 30, and 33). More than 80% of shaken babies have ocular manifestations; therefore, an appropriate ophthalmic evaluation is critical.4 Bilateral findings are present in 85% of affected children, and one fifth of surviving children have permanently poor vision.4 There may be a correlation between the severity of retinal hemorrhage and neurologic outcome.5 Perimacular retinal folds may be pathognomic.6

PEARL... Although retinal hemorrhage has occasionally been noted to occur after CPR, a prospective study failed to find a

causal relationship in nontraumatized patients.7

Examination of traumatized children can be difficult, even dangerous. Monitored sedation with ketamine, Fentanyl, and/or Versed can be helpful if administered

by an experienced ER physician or anesthesiologist. Bradyarrhythmias and episodic apnea are common in neonates and are best managed by experienced neonatologists. Photographic documentation and/or careful drawings are important for both medical and legal reasons (see Chapter 8).

Patients with Psychiatric Disease

The injury mechanism in psychiatric patients is often dramatic, historical details are inaccurate, and consent is impossible. Early recognition of the psychiatric disturbance and appropriate consultation are key to successful management.

•Oedipism (autoenucleation) is a medical emergency requiring ophthalmic and psychiatric treatment. Both eyes may be injured or enucleated. Retrobulbar hemorrhage (see Chapter 12) can ensue, for which lateral canthotomy, cantholysis, and intravenous steroids may be useful; with treatment, even NLP initial vision can improve dramatically.8 One should always consider concomitant illicit drug use and obtain a toxicology screen.

•Dementia or delirium should always be suspected in an elderly patient who suffers eye injury in a fall. Such patients need neurologic and musculoskeletal evaluations as well as close observation to reduce the risk of repeated injury.

Occult Ocular Trauma

Despite a lack of obvious signs, eye injury may be present in the polytraumatized patient; see Chapter 9 for risk factors and diagnosis.

Major Disasters in Peace and War

Terrorism-related eye injury appears to be an increasing threat (see the chapter on The patient’s perspective), and the eye is commonly involved. In the Oklahoma City bombing9 nearly 10% of survivors suffered ocular injury, most commonly corneal abrasions, lid and brow lacerations, open globe injuries, and conjunctivitis; 4% of eyes harbored IOFBs; and patients with eye injury had a higher risk of more severe systemic injuries.

In the bombing of the U.S. Air Force compound in Dahran, Saudi Arabia,10 11% of the victims had severe ocular injury.

In the 1973 Yom Kippur and 1982 Lebanon wars, almost 7% of all injuries in the Israeli Defense Force involved the eye.11

Concurrent Ocular and Orbital Injury

The timing of surgery for one injury in cases of ocular polytrauma may affect the timing of another (e.g., orbital fracture repair is deferred until the risk of rebleeding in hyphema is diminished; a “trap-door” fracture’s otherwise urgent repair12 is delayed because the globe’s rupture must be closed first; see also Chapter 8).

76 • SECTION II EMERGENCY MANAGEMENT

OPHTHALMIC CONDITIONS AS A

RESULT OF SYSTEMIC INJURIES

Traumatic Optic Neuropathy

Early identification of TON is very important. Highdose corticosteroids13 or other interventions, rather than observation,14 should be considered (see Chapter 37), although the results are not conclusive.15

Cranial Neuropathies

Acute palsy of a cranial nerve occasionally develops.

PEARL... An oculomotor nerve palsy should raise concern about a ruptured aneurysm, best imaged by digital subtraction angiography or MRI and angiography if the patient is otherwise stable. With a 25 to 50% mortality rate and severe neurologic impairment in half of the survivors, a ruptured intracranial aneurysm requires early recognition and treatment.16 The ophthalmologist’s diag-

nostic input can be critical.

REFERENCES

1.Poon A, McCluskey PJ, Hill DA. Eye injuries in patients with major trauma. J Trauma. 1999;46:494–499.

2.Sastry SM, Paul BK, Bain L, Champion HR. Ocular trauma among major trauma victims in a regional trauma center. J Trauma. 1993;34:223–226.

3.United States Department of Health and Human Services. Child Maltreatment 1998: Reports from the States to the National Child Abuse and Neglect Reporting System. Washington, DC: US Government Printing Office; 2000.

4.Odom A, Christ E, Kerr N, et al. Prevalence of retinal hemorrhages in pediatric patients after in-hospital cardiopulmonary resuscitation: a prospective study. Pediatrics. 1997;99:E3.

5.Wilkinson WS, Han DP, Rappley MD, Owings CL. Retinal hemorrhage predicts neurologic injury in the shaken baby syndrome. Arch Ophthalmol. 1989;107:1472–1474.

6.Massicotte SJ, Folberg R, Torczynski E, Gilliland MG, Luckenbach MW. Vitreoretinal traction and perimacular retinal folds in the eyes of deliberately traumatized children. Ophthalmology. 1991;98:1124–1127.

7.Kivlin JD, Simons KB, Lazoritz S, Ruttum MS. Shaken baby syndrome. Ophthalmology. 2000;107:1246–1254.

8.Wolff RS, Wright MM, Walsh AW. Attempted autoenucleation. Am J Ophthalmol. 1996;121:726–728.

9.Mines M, Thach A, Mallonee S, Hildebrand L, Shariat S. Ocular injuries sustained by survivors of the Oklahoma City bombing. Ophthalmology. 2000;107:837–843.

Purtscher’s Retinopathy

Purtscher’s retinopathy is discussed in Chapter 33.

PEARL... Rapid identification of the problems and early, coordinated treatment can reduce morbidity and increase the

quality of life for the polytraumatized patient.

SUMMARY

Perhaps the most important roles of the nonophthalmologist are early recognition of eye injury in the polytraumatized patient and appropriate early consultation. The outcome can be optimized by effective communication and planning by all specialists involved in the case. Coordinating surgeries will spare the patient the risks of multiple general anesthesias and lessen the chance of iatrogenic injury.

10.Thach AB, Ward TP, Hollifield RD, Cockerham K, Birdsong R, Kramer KK. Eye injuries in a terrorist bombing: Dhahran, Saudi Arabia, June 25, 1996. Ophthalmology. 2000;107:844–847.

11.Belkin M, Treister G, Dotan S. Eye injuries and ocular protection in the Lebanon War, 1982. Isr J Med Sci. 1984; 20:333–338.

12.Blanc JL, Cheynet F, Lagier JP, Lachard J. Trap-door fractures of the orbit floor. Apropos of 8 cases. Rev Stomatol Chir Maxillofac. 1988;89:199–203.

13.Bracken MB, Shepard MJ, Collins WF, et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study. N Engl J Med. 1990;322:1405–1411.

14.Cook MW, Levin LA, Joseph MP, Pinczower EF. Traumatic optic neuropathy. A meta-analysis. Arch Otolaryngol Head Neck Surg. 1996;122:389–392.

15.Levin LA, Beck RW, Joseph MP, Seiff S, Kraker R. The treatment of traumatic optic neuropathy: the International Optic Nerve Trauma Study. Ophthalmology. 1999;106:1268–1277.

16.Hop JW, Rinkel GJ, Algra A, van Gijn J. Case-fatality rates and functional outcome after subarachnoid hemorrhage: a systematic review. Stroke. 1997;28: 660–664.

Chemical injuries of the eye may produce extensive damage to the ocular surface and thus lead to visual impair- ment.1–4 In addition to causing ocular

surface injury, alkalies (Fig. 11–1) readily penetrate into the eye, damaging the corneal stroma and endothelium as well as other anterior segment structures (e.g., iris, lens, ciliary body). Most acids (Fig. 11–2) tend to remain confined to the ocular surface. The important agents involved in chemical injuries of the eye are summarized in Table 11–1.2,3

PEARL... Strong acids, such as hydrofluoric acid, may penetrate as readily as alkalies do, producing the same spectrum

of ocular injury.2

ETIOLOGY

The most common alkalis causing injury4 are:

•ammonia (NH3 ; a common ingredient in many household cleaning agents and causing the most serious injury);

•lye (NaOH; a common ingredient in drain cleaners and causing the most serious injury);

•potassium hydroxide (KOH);

•magnesium hydroxide (Mg[OH]2); and

•lime (Ca[OH]2 ; the most common cause, which fortunately does not inflict as much damage as rapidly penetrating alkalies do).

The most common acids causing injury4 are:

•sulfuric (H2SO4 ; the most common cause: an ingredient in automobile batteries2);

•sulfurous (H2SO3);

•hydrofluoric (HF; rapidly penetrating and causing the most serious injuries2);

•acetic (CH3COOH);

•chromic (Cr2O3); and

•hydrochloric (HCl).

EPIDEMIOLOGY AND PROGNOSIS

In the USEIR, 3.6% of all serious injuries are chemical burns. In one study5 :

•most victims were young (usually between 16 and 25 years of age) and male (76%);

•the most common sites of accidental injury were industrial premises (63%) and the home (33%);

•criminal assault was rather frequent (11%);

•alkali injuries were nearly twice as common as acid injuries; and

•only 8% of patients required hospitalization, and less than 1% suffered severe, permanent visual loss.

In another study6 :

•70% of patients were adult males, 23% were adult females, and 7% were children;

•most patients were between 16 and 45 years of age;

•industrial accidents accounted for 61% of the injuries; 37% were due to household accidents; and

•88% of the injuries were classified as mild.

FIGURE 11–1 Severe alkali injury. The entire epithelium is either absent or devitalized. Because of stromal and intraocular penetration, the corneal stroma is cloudy, in contrast to the appearance in Figure 11–2. (From Wagoner MD. Chemical injuries of the eye: current concepts in pathophysiology and therapy. Surv Ophthalmol. 1997;41:275–313, Reprinted by permission from Elsevier Science.)

FIGURE 11–2 Acid injury caused by exploding car battery. A 100% epithelial defect is present. Following débridement of necrotic epithelium (some remaining peripherally), the stroma is remarkably clear because of the function of the epithelium as a barrier to acid penetration. (From Mandel ER, Wagoner MD. Atlas of Corneal Disease. Philadelphia: WB Saunders; 1989:71. Reprinted by permission from WB Saunders.)

Mild injury with 610% concentration; severe injury with higher

Although the majority of chemical injuries are without serious sequelae, the prognosis for eyes that present with severe injuries is guarded; in one series,7 only 15% achieved adequate visual recovery.

PATHOPHYSIOLOGY

The severity of ocular injury after chemical exposure is related to:

•surface area of contact;

•depth of penetration; and

•degree of limbal stem cell injury.

into the AC can result in secondary glaucomaa and cataract.7 Irreversible damage to the ciliary body with hypotony and phthisis may follow prolonged aqueous pH levels above 11.5.11

If the external pH is restored to normal, the aqueous pH levels return to normal within 30 minutes to 3 hours, depending upon the amount of penetration.11

Limbal Stem Cell Injury

PEARL... Following corneal epithelial injury, recovery is dependent upon the

most proximal, viable epithelium.12,13

Both alkalies and acids cause the ocular surface epithelial cells to die upon contact. The surface area of contact can be assessed by examination of the fluo- rescein-staining pattern of the corneal or conjunctival epithelium.

•Complete corneal epithelial injury requires epithelium from the limbus,14–20 where the stem cells of the corneal epithelium reside (see Chapter 32).

•With extensive corneal and limbal epithelial injury, the surrounding conjunctival epithelium provides the only source for epithelial regeneration.21

PEARL... It is important to remember that retained particulate matter in the superior fornix (e.g., in case of lime plaster injury) can be a source of continued exposure of

the ocular surface to additional damage.

Depth of Penetration

PEARL... In general, alkalies tend to penetrate more effectively than acids.1–4

Penetration of alkalies and acids into the corneal stroma may result in keratocyte death and hydration of the ground substance with loss of stromal clarity.8,9 Hydration of collagen fibrils results in thickening and shortening with distortion of the trabecular meshwork and potential increase in IOP.7,8

The time to penetration into the AC varies from almost immediate after ammonia injury to 3 to 5 minutes after sodium hydroxide injury.10,11 Penetration

The clinical course of reepithelialization and its impact upon therapeutic decision making are discussed in Chapter 32.

THERAPEUTIC PRINCIPLES

A modification of our three-step approach to sterile corneal ulceration is applicable for treating the chemically injured eye from the outset.22,23

Step 1: Promote ocular surface epithelial recovery with proper phenotypic transdifferentiation.

PEARL... The recovery of an intact and phenotypically normal corneal epithelium is the most important determinant of a

favorable outcome following chemical injury.

a See Chapter 20 for the treatment of glaucoma in chemical injuries.

80 • SECTION II EMERGENCY MANAGEMENT

•Débridement of necrotic epithelium (Fig. 11–2) allows subsequent migration of adjacent viable epithelium into the denuded area.

•Nonpreserved topical lubricants may facilitate reepi-thelialization in older patients with aqueous tear deficiency. In young patients with adequate tear production, tear supplementation is not necessary.

•Pressure patching and/or bandage soft contact lens therapy does not improve the rate of reepithelialization but may provide pain relief.

Subsequent medical and surgical interventions to enhance corneal epithelial recovery are discussed in Chapter 32.

Step 2: Apply supportive repair (augment collagen production and/or minimize collagenase activity)

Aqueous levels of ascorbateb may be depleted following chemical injuries with intraocular penetration, due to impaired secretion by the ciliary body epithelium.24–26

The beneficial effects of supplemental topical and systemic ascorbate in facilitating collagen synthesis and reducing the risk of corneal ulceration due to excessive collagenolysis are achieved with early supplementation; when corneal ulceration begins, supplemental ascorbate is of limited benefit in halting its progression.24–26

Collagenase inhibitors were used earlier27 but, being ineffective, have been abandoned.

The efficacy of tetracycline derivatives in preventing corneal ulceration after chemical injury is maximized with early administration. They have been shown to be efficacious in:

•reducing collagenase activity;28

•inhibiting polymorphonuclear leukocyte activity;29 and

•inhibiting corneal ulceration30 in experimental alkali injuries.

b A cofactor in the rate-limiting step of collagen synthesis; its deficiency may contribute to the impairment of corneal repair after chemical injury.

PEARL... Therapeutic strategies that exclude polymorphonuclear and mononuclear leukocytes from the stroma contribute to prevention and arrest of corneal

ulceration.31,32

Step 3: Control inflammation

Citrate,c a naturally occurring vitamin, reduces leukocyte infiltration into the stroma and the incidence of corneal ulceration experimentally—provided that it is administered early.26,35,d

Corticosteroids reduce inflammatory cell infiltration and stabilize polymorphonuclear leukocyte cytoplasmic and lysosomal membranes.36 The key to successful use of corticosteroids is to maximize their anti-inflammatory effect during the first week, when the risk-benefit ratio is favorable. There is little risk37 of sterile ulceration in the first week following severe chemical injury whether or not corticosteroids are used. Corticosteroids interfere with stromal wound repair by impairing both keratocyte migration into the area of injury and collagen syn- thesis,38–40 but their deleterious side effect does not become apparent until corneal repair processes begin after 10 to 14 days.e

Modifications of topical inflammatory therapy after the first week are discussed in Chapter 32.

SPECIFIC THERAPY

The specific therapeutic strategies employed immediately after injury focus upon:

• elimination of residual alkali or acid from the eye;

cA calcium chelator that decreases the membrane and intracellular calcium levels of polymorphonuclear leukocytes, with resultant impaired chemotaxis, phagocytosis, adherence, and release of lysosomal enzymes.33,34

dSimilarly to ascorbate, it has no effect on the progression of established corneal ulceration.

eAfter 7 to 10 days, the suppression of keratocyte collagen production by corticosteroids may offset the advantages of their effect on inflammatory cell suppression and collagenase inhibition, resulting in a net shift of corneal repair toward ulceration.

•institution of topical and systemic medical therapy to minimize adverse sequelae.

Subsequent medical therapy and surgical intervention are discussed in Chapter 32.

2.Evert the upper lid (see Chapter 13 for the technique) and irrigate the fornices.

PEARL... Use of topical anesthetics and lid retractors is very helpful; use of an

intravenous infusion set provides convenience.

S P E C I A L C O N S I D E R A T I O N

Chemical injury is an absolute emergency in which literally every second counts. Intervention must precede the steps of a traditional examination such as detailed history taking or even recording the visual acuity (see Chapter 9).

Irrigation

PEARL... The physician must assume that any previous irrigation was inadequate and thus copious irrigation should be

resumed immediately.

One of the main determinants of the ultimate outcome following chemical injury is the duration of contact between the chemical agent and the eye. Because of the deep location and relatively protected site of the limbal stem cells, their injury may be averted with prompt irrigation. Follow these steps given below.

1.Irrigate copiously

•No therapeutic differences have been identified between normal saline, normal saline with bicarbonate, lactated Ringer’s, balanced salt solution (BSS), and BSS-plus.41

•Try to use other neutral fluids.f

•As it is impossible to “overirrigate” a chemically injured eye, irrigation for 15 to 30 minutes is recommended.

3.Check the pH a few minutes after irrigation; continue irrigating until the pH reaches 7.0.

4.Remove remnants of the agent (e.g., plaster) from the fornices mechanically with a moistened cottontippedg applicator or a jeweler’s forceps. Double eversion (see Chapter 13) provides the best access to the upper fornix.

The benefit of paracentesis and irrigation of the AC following a severe chemical injury is uncertain.42

Débridement

Necrotic corneal epithelium should be débrided to allow proper migration of adjacent, viable epithelium.

Devitalized conjunctival epithelium should also be débrided to remove a nidus of persistent inflammation, which can also retard corneal reepithelialization.43

Medical Therapy

See the preceding rationale for the subsequent use of topical and systemic medications; the specific recommended dosages are listed in Table 11–2. Topical

TABLE 11–2 TOPICAL AND SYSTEMIC MEDICATIONS TO BE

USED AT THE OUTSET IN THE TREATMENT OF MODERATE AND

SEVERE CHEMICAL INJURIES

82 • SECTION II EMERGENCY MANAGEMENT

sodium ascorbate and citrate are not available commercially but can be prepared by most pharmacy departments.

SUMMARY

Chemical injuries of the eye are true ocular emergency. The most important aspect in the manage-

REFERENCES

ment of these injuries is to begin prompt and copious irrigation of the eye. Following this, the management is less emergent and focuses on the promotion of ocular surface recovery and ocular repair. The ultimate outcome of these injuries is determined, in large part, by the nature of the chemical agent and the duration of contact between that noxious agent and the eye.

1.Hughes WF. Alkali burns of the cornea. I. Review of the literature and summary of present knowledge. Arch Ophthalmol. 1946;35:423–426.

2.McCulley JP. Chemical injuries. In: Smolin G, Thoft RA, eds. The Cornea: Scientific Foundation and Clinical Practice. 2nd ed. Boston: Little, Brown; 1987:527–542.

3.Wagoner MD, Kenyon KR. Chemical injuries of the eye. In: Albert DM, Jakobiec FA, eds. Principles and Practice of Ophthalmology: Clinical Practice. Vol 1. Philadelphia: WB Saunders; 1994:234–245.

4.Wagoner MD. Chemical injuries of the eye: current concepts in pathophysiology and therapy. Surv Ophthalmol. 1997;41:275–313.

5.Morgan SJ. Chemical burns of the eye: causes and management. Br J Ophthalmol. 1987;71:854–857.

6.Kuckelkorn R, Luft I, Kotteck AA, et al. Chemical and thermal eye burns in the residential area of RWTH Aachen. Analysis of accidents in 1 year using a new automated documentation of findings. Klin Monatsbl Augenheilkd. 1993;203:34–42.

7.Kuckelkorn R, Makropoulos W, Kotteck A, Reim M. Retrospective study of severe alkali burns of the eye.

Klin Monatsbl Augenheilkd. 1993;203:397–402.

8.Matsuda H, Smelser GK. Epithelium and stroma in alkali-burned corneas. Arch Ophthalmol. 1973;89:396–401.

9.Matsuda H, Smelser GK. Endothelial cells in alkaliburned corneas; ultrastructural alterations. Arch Ophthalmol. 1973;89:402–409.

10.Grant WM. Experimental investigation of paracentesis in the treatment of ocular ammonia burns. Arch Ophthalmol. 1950;44:399–404.

11.Paterson CA, Pfister RR, Levinson RA. Aqueous humor pH changes after experimental alkali burns. Am J Ophthalmol. 1975;79:414–419.

12.Friedenwald JS, Buschke W. Some factors concerned in the mitotic and wound-healing activities of the corneal epithelium. Trans Am Ophthalmol Soc. 1944; 42:371–383.

13.Kuwabara T, Perkins DG, Cogan DG. Sliding of the epithelium in experimental corneal wounds. Invest Ophthalmol. 1976;15:4–14.

14.Davanger M, Evensen A. Role of the pericorneal papillary structure in renewal of corneal epithelium. Nature. 1971;229:560–561.

15.Friend J, Thoft RA. Functional competence of regenerating ocular surface epithelium. Invest Ophthalmol Vis Sci. 1978;17:134–139.

16.Thoft RA, Friend J, The X, Y, Z hypothesis of corneal epithelial maintenance. Invest Ophthalmol Vis Sci. 1983;24:1442–1443.

17.Buck RC. Measurement of centripetal migration of normal corneal epithelial cells in the mouse. Invest Ophthalmol Vis Sci. 1985;26:1296–1299.

18.Schermer A, Galvin S, Sun TT. Differentiation-related expression of a major 64K corneal keratin in vivo and in culture suggests limbal location of corneal epithelial stem cells. J Cell Biol. 1986;103:49–62.

19.Zieske JD, Bukusoglu G, Yankauckas MA. Characterization of a potential marker of corneal epithelial stem cells. Invest Ophthalmol Vis Sci. 1992;33:143–152.

20.Thoft RA, Wiley LA, Sundarraj N. The multipotential cells of the limbus. Eye. 1989;3(2):109–113.

21.Shapiro MS, Friend J, Thoft RA. Corneal re-epithelial- ization from the conjunctiva. Invest Ophthalmol Vis Sci. 1981;21:135–142.

22.Kenyon KR. Decision making in the therapy of external eye disease: noninfected corneal ulcers. Ophthalmology. 1982;89:44–51.

23.Wagoner MD, Kenyon KR. Noninfected corneal ulceration. In: Focal Points: Clinical Modules for Ophthalmologists. Vol 3. San Francisco: American Academy of Ophthalmology; 1985:7.

24.Pfister RR, Paterson CA. Additional clinical and morphological observations on the favorable effect of ascorbate in experimental ocular alkali burns. Invest Ophthalmol Vis Sci. 1977;16:478–487.

25.Pfister RR, Paterson CA. Ascorbic acid in the treatment of alkali burns of the eye. Ophthalmology. 1980;87: 1050–1057.

26.Pfister RR, Haddox JL, Lank KM. Citrate or ascorbatecitrate treatment of established corneal ulcers in the alkali injured rabbit eye. Invest Ophthalmol Vis Sci. 1988;29:1110–1115.

27.Brown SI, Hook CW. Treatment of corneal destruction with collagenase inhibitors. Trans Am Acad Ophthalmol Otolaryngol. 1971;75:1199–1207.

28.Golub LM, McNamara TF, D’Angelo G, Greenwald RA. A nonantibacterial chemically-modified tetracycline inhibits mammalian collagenase activity. J Dent Res. 1987;66:1310–1314.

29.Gabler WL, Creamer HR. Suppression of human neutrophil functions by tetracyclines. J Periodont Res. 1991;26:52–58.

30.Perry HD, Hodes LW, Seedor JA, et al. Effect of doxycycline hyclate on corneal epithelial wound healing in the rabbit alkali-burn model. Preliminary observations. Cornea. 1993;12:379–382.

31.Kenyon KR. Inflammatory mechanisms in corneal ulceration. Trans Am Ophthalmol Soc. 1985;83:610–663.

32.Kenyon KR, Berman M, Rose J, Gage J. Prevention of stromal ulceration in the alkali-burned rabbit cornea by glued-on contact lens. Evidence for the role of polymorphonuclear leukocytes in collagen degradation.

Invest Ophthalmol Vis Sci. 1979;18:570–587.

33.Paterson CA, Williams RN, Parker AW. Characteristics of polymorphonuclear leukocyte infiltration into the alkali-burned eye and influence of sodium citrate. Exp Eye Res. 1984;39:701–708.

34.Pfister RR, Haddox JL, Dodson RW, Deshazo WF. Polymorphonuclear leukocyte inhibition by citrate, other

heavy metal chelators, and trifluoperazine: evidence to support calcium binding protein involvement. Invest Ophthalmol Vis Sci. 1984;25:955–970.

35.Haddox JL, Pfister RR, Yuille-Barr D. The efficacy of topical citrate after alkali injury is dependent on the period of time it is administered. Invest Ophthalmol Vis Sci. 1989;30:1062–1068.

36.Basu PK, Avaria M, Jankie R. Effect of hydrocortisone on the mobilisation of leucocytes in corneal wounds. Br J Ophthalmol. 1981;65:694–698.

37.Donshik PC, Berman MB, Dohlman CH, et al. Effect of topical corticosteroids on ulceration in alkali-burned corneas. Arch Ophthalmol. 1978;96:2117–2120.

38.Beams R, Linabery L, Grayson M. Effect of topical corticosteroids on corneal wound strength. Am J Ophthalmol. 1968;66:1131–1133.

39.Gasset AR, Lorenzetti DW, Ellison EM, Kaufman HE. Quantitative corticosteroid effect on corneal wound healing. Arch Ophthalmol. 1969;81:589–591.

40.Phillips K, Arffa R, Cintron C, et al. Effects of prednisolone and medroxyprogesterone on corneal wound healing, ulceration, and neovascularization. Arch Ophthalmol. 1983;101:640–643.

41.Herr RD, White GL Jr, Bernhisel K, et al. Clinical comparison of ocular irrigation fluids following chemical injury. Am J Emerg Med. 1991;9:228–231.

42.Burns RP, Hikes CE. Irrigation of the anterior chamber for the treatment of alkali burns. Am J Ophthalmol. 1979;88:119–120.

43.Wagoner MD, Kenyon KR, Gipson IK, et al. Polymorphonuclear neutrophils delay corneal epithelial wound healing in vitro. Invest Ophthalmol Vis Sci. 1984;25: 1217–1220.

Patients presenting to the ophthalmologist with eyelid and/or orbital trauma (Fig. 12–1) may also have systemic injuries, which usually take precedence

over the ophthalmic evaluation (see Chapters 9 and 10).

EVALUATION

Assessment of the orbit and the adnexa begins with a focused ophthalmic history; the mechanism by which the injury was inflicted helps direct the physical examination.

FIGURE 12–1 Dramatic ocular injury following a horse kick. Associated injuries include multiple bone fractures.

PEARL... Injuries caused by highspeed missiles or metal-on-metal contact increase the likelihood of an eyelid or intraorbital foreign body. Blows to the orbit by large objects can lead to orbital bone fractures. Dog bite injuries in the medial canthus are often

associated with canalicular lacerations.

Evaluation of the adnexa begins with the eyelid and canalicular systems; and usually precedes detailed examination of the eyes.

PEARL... Evidence of laceration in the medial canthal area requires nasolacrimal duct probing and irrigation. Failure to diagnose

the canalicular laceration can lead to lifelong tearing.1 Remember that canalicular lacerations can result from a deceptively small eyelid laceration.

Assessing the eyelid position and function in the ER requires measurement and documentation of lid position and excursions. Lid lacerations may cause a dramatic ptosis, but lid function may dictate the method of repair. Traumatic ptosis may be present without eyelid laceration. Eyelid edema, burns, and preseptal cellulitis all compromise eyelid function, and their documentation is important.

Extraocular muscle function is assessed to evaluate the presence of restricted movement. Restricted muscle function is a hallmark of:

•blowout fracture;

•orbital cellulitis; or

•orbital foreign body.

Progressive orbital signs and symptoms require expedited radiographic examination.a A CT scan with axial and coronal cuts best demonstrates the relationship between orbital bones and soft tissue.

EMERGENCY CONDITIONS AND THEIR

MANAGEMENT

The repair of full-thickness eyewall injury always takes precedence over the repair of periocular trauma; repair of orbital bone damage can usually be delayed for weeks.2

P I T F A L L

The repair of a blowout fracture at the time of open globe repair is contraindicated.

True orbital or periocular emergencies are life or vision threatening. Fortunately, they are infrequent and include:

•expanding orbital hemorrhage;

•orbital abscess; and

•certain types of orbital foreign bodies (e.g., pressing on the optic nerve, protruding) (Fig. 12–2).

aNot required in case of a straightforward orbital blowout fracture.

Orbital hemorrhages are often iatrogenic, caused by retrobulbar injections or eyelid surgery. Depending on the severity of the condition, signs include:

•sudden proptosis;

•hemorrhagic chemosis;

•vision loss;

•elevated IOP/reduced or absent retinal perfusion;

•restricted extraocular muscle movements;

•APD; and

•asymmetrical color vision.

Medical treatment (for less severe cases) includes:

•mannitol;

•steroids; and

•antiglaucoma drops.

The surgical management options are:

•lateral cantholysis;

•evacuation of hemorrhage;

•paracentesis; and

•bony orbital decompression.

Orbital abscess is most frequently caused by spread of a preexisting sinus infection (Fig. 12–3). In severe cases, vision may be compromised. Classic signs3 include:

•proptosis;

•restricted extraocular muscle movement;

•fever; and

•malaise.

The surgical planning for drainage of an orbital abscess requires a radiological examination; a CT scan with axial and coronal cuts is the first choice and contrast material often aids in the identification of the orbital abscess (Fig. 12–4). MRI is a second choice. The treatment involves surgical drainage and systemic antibiotics.

Orbital foreign bodies do not always require (emergency) removal. Metallic objects (e.g., BB, shotgun

FIGURE 12–2 Retained wooden orbital foreign body.

FIGURE 12–3 Orbital abscess associated with proptosis, restricted extraocular muscle movement, fever, and malaise.

86 • SECTION II EMERGENCY MANAGEMENT

FIGURE 12–4 Superior orbital abscess, left side.

pellet) or glass buried deep in the orbit not only may be safely left in place, but their aggressive removal can lead to complications. Conversely, immediate removal is required for:

•protruding foreign bodiesb ; and

•objects pressing on the optic nerve.

Periocular Damage

These injuries rarely require urgent intervention; they must be adequately assessed and a treatment plan designed. It is usually possible to treat in the ERc :

bDo not simply pull out a protruding foreign body in the ER; it is usually wiser to remove the object in the well-equipped operating room.

cThe inability of the patient to cooperate, the lack of equipment, and the technically challenged physician are reasons to consider repairing eyelid lacerations in the operating room instead.

•eyelid lacerations;

•puncture wounds; and

•abrasions.

PEARL... Eyelid margin lacerations and canalicular lacerations require meticulous repair. If they can be safely protected, the treatment may be delayed for 48 hours or less because they are best repaired in the operating room. Clean eyelid and canalicular lacerations can be pressure patched over an antibiotic ointment, and reliable patients may be discharged until definitive repair later in the hospital. For patients with poor reliability, admission to the hospital is recommended. Antibiotics should be given if surgery is delayed; tetanus prophylaxis should also be considered (see Chapter 8 and

the Appendix).

Repair of Pediatric Eyelid Trauma

Children are best treated in the operating room, not in the ER: eyelid margin repair requires accurate, precise, suture placement. The close proximity of the globe makes needle passes dangerous if restraints have to be used for lack of cooperation.

SUMMARY

Blunt and sharp forces can lead to severe periocular injuries. It is important to rule out concomitant ocular injury, particularly open globe injury, since management of injury to the globe often takes precedence over injury to the lids or orbit. Periocular injuries rarely require urgent repair, but instead should be adequately assessed and a plan designed.

1.Baylis HI, Axelrod R. Repair of the lacerated canaliculus. Ophthalmology. 1978;84:1271–1276.

2.Hawes MJ, Dortzbach RK. Surgery on orbital floor fractures. Influence of time of repair and fracture size. Ophthalmology. 1983;90:1066–1070.

3.Korhel GB, Krauss HR, Winnik J. Orbital abscess: presentation, diagnosis, therapy and sequelae. Ophthalmology. 1982;89:492–498.