Ocular Trauma - Banta

1
Epidemiology and economic

impact of ocular trauma
James T. Banta
EPIDEMIOLOGY OF OCULAR TRAUMA

3. 200 000 open globe injuries occur annually
Make no mistake, ocular trauma is a disease. It 4. 19 million people are unilaterally blind, 2.3
has a well-established natural history, modifiable million have bilateral low vision, and 1.6
risk factors, and distinct prevention, classifica- million are bilaterally blind due to eye
tion, and treatment schemes. The literature is injuries.
replete with reports of ocular trauma, both visu- The lifetime prevalence of eye injury in three
ally significant and insignificant. Unfortunately, large epidemiologic studies was approximately
the vast majority of these studies are hampered 20%.4,15,16 Interestingly, a person with an eye
by their retrospective nature and extrapolation to injury is three times more likely to have a second
larger, often very different populations. However, eye injury.4 After spending 5 years in an eye
when the ocular trauma literature is viewed as a emergency room, I can defi nitively say that
whole, multiple aspects are incredibly consistent: ocular trauma is a recurrent disease. It is remark-
1. Ocular trauma is a disease with a bimodal age able how often a patient with a metallic corneal
distribution, the fi rst in the years of late ado- foreign body has multiple corneal scars from pre-
lescence and early adulthood and the second vious foreign body removals. Similarly, assault-
in those older than 70.1–3 related trauma, particularly fi st-fighting, has a
2. Ocular trauma, particularly severe, vision- distinct pattern of recurrence.
threatening eye injuries, affects men three to Severe eye trauma may slowly be decreasing in
five times as frequently as women.1,3–8 incidence in large part due to improved safety
3. Ocular trauma is a significant cause of visual standards in the workplace. However, it is clear
loss, especially in lower socioeconomic strata that current prevention strategies are woefully inad-
and underdeveloped countries.5,9,10 equate. Studies have shown that appropriate eye
4. Ocular trauma is largely preventable, espe- protection is rarely in place at the time of a
cially in the workplace.6,11–13 severe eye injury.6,11–13 A study in Singapore
5. Ocular trauma is a recurrent disease.4 revealed a troubling trend.13 Of a cohort of eye
A large worldwide meta-analysis of eye injury injuries seen in an emergency department, 71.4%
epidemiology was performed by the World were work-related. Of these work-related cases,
Health Organization and published in 1998.14 21.7% wore eye protection, 43.7% were given eye
The analysis compiled information from various protection but did not use it, and 34.6% were
studies performed between 1971 and 1995. not provided eye protection. A study in the
Several salient points emerged: United States of open globe injuries suffered at
1. 55 million eye injuries which restrict activities work discovered a mere 6% wore eye protection
for ≥ 1 day occur annually at the time of injury.11
2. 750 000 eye injuries require hospitalization Cases of eye injuries requiring hospitalization
annually have also declined in the last decade, not because
1
Ocular trauma
Table 1.1 Physical characteristics of various sporting balls commonly encountered in

ocular trauma
Ball type Diameter Max velocity Weight Distensibility

Baseball 7.62 cm >150 kph 145 g Minimal
Tennis ball 6.5 cm >150 kph 57 g Moderate
Racquetball 5 cm >150 kph 40 g Significant
Hockey puck 2.54 cm vertical >150 kph 160 g None

7.62 cm horizontal
Paintball pellet 1.72 cm 90–150 mps 3.2 g Significant
cm = centimeter, kph = kilometers per hour, mps = meters per second, g = grams.
of a major decrease in the number of severe eye 3.5 × 4.0 cm. Use of a ball, projectile, or playing
injuries, but because of changing indications object (e.g. stick, bat, racket) small enough to fit
for hospitalization.2 Patients with a traumatic within the orbit greatly increases the risk of
hyphema, now typically observed on an outpa- severe eye injury (Table 1.1). Eye injuries have
tient basis, were routinely hospitalized for 5–7 been described in virtually every major and
days in years past. Likewise, the frequency and minor sport. The most common and devastating
duration of hospitalization for open globe inju- offenders are hockey, racket sports, baseball, and
ries has decreased. more recently, paintball (often referred to as
Ocular trauma in children has been exten- ‘war games’). In our recent experience, paintball
sively studied. During the fi rst few years of life, injuries are rapidly becoming the most common
the incidence of ocular injury is essentially equal and severe of the sports-related ocular injuries
in males and females, but changes quickly to the encountered (Figure 1.1). The number of patients
male preponderance seen in adults.10 The major- and severity of injury encountered with this
ity of injuries occur at home or school.17–19 Lower activity is rapidly moving into the realm of a
socioeconomic and educational standing seem to public health crisis. As will be discussed in the
increase the risk of injury.10 Adult supervision following chapter, certain sports have shown a
clearly decreases the incidence of eye injuries in dramatic reduction in the number of eye injuries
children.10,18 Scissors and furniture were found when the proper eye protection is utilized.
to be frequent causes of severe eye injuries in Motor vehicle accidents (MVA) are another
children less than 6 years old, while toys, balls, source of eye injury that has been individually
and stones were more frequently implicated in examined. The question has arisen, ‘Do airbags
children 6 years of age or older.17 Following increase the rate of ocular injury during a motor
ocular injury in children, the rate of blindness vehicle accident?’ Confl icting results are found
(visual acuity <20/200) ranges from 1% to in the literature. A large study that reviewed
34%.10,19–21 22 236 MVA with frontal airbag deployment
Sports activities are a significant cause of ocular found an increase in minor eye injuries (specifi-
trauma. The protective bony orbit measures cally corneal abrasions) and a decrease in severe
2
Epidemiology and economic impact of ocular trauma
in 1985 and published in 1988.26 The direct cost,

excluding physician fees and laboratory exams,
was $2400 for a traumatic hyphema and $6300
for an open globe injury. A conservative estimate
of total direct and indirect cost of all ocular
injuries in this eye emergency department for
1 year was $5 million and a loss of 60 work
years. Taking into account inflation and the small
population studied, the overall costs when
considered on a global scale are staggering. An
estimate of the national total for direct hospital
costs, extrapolated from information obtained
Figure 1.1 An 11-year-old boy was struck with a from California hospitals during a 1-year period,
paintball pellet leading to hyphema and extensive iris was $99.7 million for the year 2000.27 As large
disruption. as this number is, it only represents a small frac-
tion of the cost when physician fees, laboratory
and radiologic exams, drugs, rehabilitation, and
eye injuries.22 A study out of Henry Ford Hospi- particularly lost work days are taken into
tal found the rate of MVA-related ocular injuries account.
was reduced by the use of airbags, as was the It is clear that prevention of severe eye injuries
death rate.23 A large meta-analysis published in is an accomplishable goal and one that demands
2003 found the risk of a severe eye injury due to attention given its far-reaching societal and eco-
airbag deployment to be 0.4%.24 The most recent nomic impact. Ocular trauma is a public health
epidemiologic study showed a two-fold increase problem with identifiable prevention strategies.
in eye injuries with airbags and a two-fold The following chapter will review these preven-
decrease in eye injuries with seatbelt use.25 In tion strategies in detail.
short, it appears that although airbags may
increase the overall rate of eye injuries, the
protective effect against severe eye injuries, and FUTURE DIRECTIONS
particularly death, outweighs the small risk.
Compiling epidemiologic data on ocular trauma
ECONOMIC IMPACT OF is a vital part of defi ning populations, risk factors,
OCULAR TRAUMA and trends in this disease state. The World
Eye Injury Registry (WEIR) was established to
What is the economic impact of ocular trauma? collect information from ophthalmologists on
Simply put, immense. It is difficult to quantify severe, vision-threatening eye injuries. Standard-
precisely because of the significant impact of ized reporting forms are used to capture data at
indirect costs, particularly lost work days. Only the initial visit (Figure 1.2) and 6 months after
a few studies looking at the economic impact of the initial injury. The standardized nature of the
ocular trauma have been published. information gathered allows accurate compari-
An epidemiologic study of eye trauma at an sons to be made. Further information is available
urban eye emergency department was conducted online at www.WEIRonline.org.
3
WORLD EYE INJURY REGISTRY
INITIAL REPORT
1) Check appropriate responses 2) Fill out comments 3) File bilateral injury reports seperately
4) Submit Data via WEIRONLINE.org 5) Write Down Record ID _________________________
M INITIAL DIAGNOSES:
A I D E N T I F I C AT I O N : I SOURCE:
OPEN GLOBE INJURY: Yes 18.5 Postequatorial Extension No
Patient’s Initials: __________________ 00 Hammer on Metal
10 Sharp Object* LACERATION: 00.0 Perioc. 02.0 Lacrim. 08.1 Contusion
Patient’s Home ZIP: _______________
11 Nail PARTIAL THICKNESS WOUND: 09.1 Corneal 09.2 Scleral
Medical Rec. #____________________ 25 Fall CORNEAL BURN: 12.0 Thermal 12.1 Alkal. 12.2 Acid
Age: _________ Sex: M F 20 Blunt Object* RUPTURE: 10.3 Corneal ______ mm 18.3 Scleral ______ mm
30 Gunshot 13.3 Corneoscleral ______ mm
Injury Date: ______/_______/_______
31 BB/Pellet Gun
Eye: Right Left PENETRATING INJURY:
40 Motor Vehicle Crash
10.4 Corneal _____mm 18.4 Scleral _____mm 13.4 Corneoscleral _____mm
Race:___________________________ 50 Fireworks*
IOFB: 90.0 Magnetic 90.1 Ant. Segment 90.2 Post. Segment
Initial Rx MD: ____________________ 60 Burn
91.0 Nonmagnetic 91.1 Ant. Segment 91.2 Post. Segment
70 Explosion
Initially Treated At:_________________ PERFORATING INJURY: 18.2 Perforating Injur y 18.21 Corneoscleral
90 Lawn Equipment*
Reporting MD: ___________________ 98 Unknown 18.22 Scleroscleral
Exam Date for Report: 99 Other* UVEA IN WOUND: 18.1 Scleral 10.1 Cornea 11.1 In Visual Axis
_______/________/________ *Description of Source: ___________ WOUND DEHISCENCE: 19.0 HYPHEMA: 20.0 _______%
Report Filer’s Name: _______________ ______________________________ IRIS PUPIL: 22.0 Iris Laceration/Dialysis 22.3 Afferent Pupil Defect
J TISSUES INVOL V E D : IOP: 24.0 Angle Recession 26.0 Glaucoma, Secondary 28.0 Hypotony
_____________________________
00 Lids LENS: 30.0 Cataract (Traumatic) 32.0 Subluxed Lens 32.1 Dislocated Lens
Contact for 6 mo F/U: ______________
09 Lacrimal System VITREOUS: 40.0 Hemorrhage 42.0 Penetration
_____________________________ 10 Cornea
RETINA: 50.0 Retinal Hemorrhage 55.5 Macular Hemorrhage
AA B I L ATERAL INJURY: Yes No 19 Sclera
51.0 Retinal Edema 55.2 Macular Edema 52.0 Retinal Defect
B EYE PROTECTION: 20 Iris 52.1 Tear 52.2 Giant Tear 52.3 Laceration 52.4 Dialysis
Yes No Unknown 22 Anterior Chamber 53.0 Retinal Detachment Number of Quadrants? 1 2 3 4
Regular Safety Sun 30 Lens
RD TYPE: 53.1 Hemorrhagic 53.2 Tract. 53.3 Rhegm. 53.5 Macular
Glass Shattered? Yes No 40 Vitreous
50 Retina CHOROID: 58.0 Hemorrhage 58.1 Rupture
Unknown
55 Macula OPTIC NERVE INJURY: 82.0 Optic Nerve
C PATIENT A BYSTANDER:
Yes No Unknown 58 Choroid ORBITAL: 70.0 Fracture 71.0 Foreign Body 73.0 Hemorrhage
D W O R K - R E L ATED:
60 Extraocular Muscle INFLAMMATION: 95.0 Uveitis 92.0 EndophthalmitisOrganism:_________________
70 Orbit
YesList Occupation below 99.0 Other or comments: ______________________________________________
80 Optic Nerve
No Unknown _____________________________________________________________________
99 Other*
Occupation: ___________________ N INITIAL OPERAT I O N : Date: ______/______/______
*Describe: _____________________
E PLACE: REPAIR EYELID WOUND: 00.0 Full-thickness 00.1 Partial-thickness
______________________________
01 Industrial Premises
K VISION (OF BOTH EYES): REPAIR LACRIMAL: 02.0 GLOBE: 18.0 Exploration of Globe
05 Farm
10 Home DATE:______/______/______ REPAIR CORNEAL: 10.4 Laceration 10.3 Rupture
20 School RE LE REPAIR SCLERAL: 18.4 Laceration 18.3 Rupture
30 Place for Recreation & Sport* 00- - - - - - NLP - - - - - 00 REPAIR CORNEOSCLERAL: 13.4 Laceration 13.3 Rupture
40 Street and Highway* 10 - - - - - - LP - - - - - - 10 IOFB: 90.1 IOFB Removal by Magnet from Anterior Segment
60 Public Building* 20- - - - - - HM - - - - - - 20 90.2 IOFB Removal by Magnet from Posterior Segment
98 Unknown 30 1/200 to 4/200 (CF) 30 91.1 IOFB Removal by Forceps from Anterior Segment
99 Other* 40- - 5/200 to 19/200 - - 40 91.2 IOFB Removal by Forceps from Posterior Segment
*Specify: _____________________ CORNEA: 19.2 Corneal Transplant 19.3 Temporary Keratoprosthesis (TKP)
____ If > 19/200 Specify Accuity ____
F I N J U R Y’S ZIP: __________________ 91 - - - Not Tested - - - 91 REPAIR WOUND DEHIS: 19.0 Dehiscence HYPHEMA: 20.0 Removal
G I N T E N T: 52 Unintentional 98- - - - Unknown - - - - 98 IRIS: 22.0 Iridectomy 22.1 Iridoplasty 22.2 Iridotomy
50 Assault 98 Unknown 99 - - - - - Other - - - - - 99 LENS: 30.0 ECCE 30.2 Phaco 30.3 Pars Plana Lensectomy
KK EYE NORMAL PRIOR TO INJURY?
51 Self-inflicted (intentional) IOL: 36.1 AC 36.2 PC
H DRUG USE:
Yes Unknown
Y N Unknown VITRECTOMY MECHANICAL: 44.0 Anterior 44.1 Posterior
Describe:______________________ No (Explain) _________________ VITRECTOMY OPEN-SKY: 44.2
ALCOHOL USE: Yes No ______________________________ ANTIBIOTICS: 45.0 Intravitreal 45.1 Intracameral
L C O M M E N T S : (Please describe the injury
Unknown RD PROPHYLAXIS: 53.0 Cryopexy 53.1 Laser 53.2 Buckle
as much as possible):
RD REPAIR: 53.01 Cryopexy 53.11 Laser 53.5 Buckle 53.3 Vitrectomy
______________________________________________________________________ 53.7 Air 53.4 Gas 53.6 Silicone Oil 53.8 Pneumatic Retinopexy
______________________________________________________________________ REPAIR EXTRAOCULAR MUSCLE: 60.0

ORBIT: 70.0 Fract. Repair 71.0 FB Removal 75.0 Decomp.
______________________________________________________________________
93.0 Evisceration 94.0 Enucleation 97.0 None 98.0 Unknown
______________________________________________________________________ OTHER: 99.0 Other or Comments:_________________________________________
Rev. 10/3/2000
______________________________________________________________________ _____________________________________________________________________
Figure 1.2 World Eye Injury Registry (WEIR) standardized reporting form for severe ocular trauma. (Data provided
by the United States Eye Injury Registry of the American Society of Ocular Trauma, through funding by the Helen
Keller Foundation, Birmingham, Alabama, USA.)
4
Epidemiology and economic impact of ocular trauma
REFERENCES 14. Négrel AD, Thylefors B. The global impact of eye injuries.
Ophthalmic Epidemiol 1998;5:143–169.
15. McCarty CA, Fu CLH, Taylor HR. Epidemiology of ocular
1. Klopfer J, Tielsch JM, Vitale S, et al. Ocular trauma in the
trauma in Australia. Ophthalmology 1999;106:1847–1852.
United States: eye injuries resulting in hospitalization,
16. Katz J, Tielsch JM. Lifetime prevalence of ocular injuries
1984 through 1987. Arch Ophthalmol 1992;110:838–842.
from the Baltimore Eye Study. Arch Ophthalmol 1993;111:
2. Tielsch JM, Parver L, Shankar B. Time trends in the incidence
1564–1568.
of hospitalized ocular trauma. Arch Ophthalmol 1989;107:
17. Tomazzoli L, Renzi G, Mansoldo C. Eye injuries in childhood:
519–523.
a retrospective investigation of 88 cases from 1988 to 2000.
3. Wong TY, Tielsch JM. A population-based study on the
Eur J Ophthalmol 2003;13:710–713.
incidence of severe ocular trauma in Singapore. Am J
18. Serrano JC, Chalela P, Arias JD. Epidemiology of childhood
Ophthalmol 1999;128:345–351.
ocular trauma in a northeastern Columbian region. Arch
4. Wong TY, Klein BEK, Klein R. The prevalence and 5-year
Ophthalmol 2003;121:1439–1445.
incidence of ocular trauma, the Beaver Dam Eye Study.
19. MacEwen CJ, Baines PS, Desai P. Eye injuries in children: the
Ophthalmology 2000;107:2196–2202.
current picture. Br J Ophthalmol 1999;83:933–936.
5. Abraham D, Vitale S, West S, Isseme I. Epidemiology of eye
20. Mela EK, Georgakopoulos CD, Georgalis A, et al. Severe ocular
injuries in rural Tanzania. Ophthalmic Epidemiol 1999;2:85–94.
injuries in Greek children. Ophthalmic Epidemiol
6. May DR, Kuhn FP, Morris RE, et al. The epidemiology of
2003;10:23–29.
serious eye injuries from the United States Eye Injury Registry.
21. Vasnaik A, Battu RR, Kurian M, George S. Mechanical eye
Graefe’s Arch Clin Exp Ophthalmol 2000:238:153–157.
(globe) injuries in children. J Ped Ophthalmol Strab
7. Glynn RJ, Seddon JM, Berlin BM. The incidence of eye injuries
2002;39:5–10.
in New England adults. Arch Ophthalmol 1998;106:785–789.
22. Duma SM, Jernigan MV, Stitzel JD, et al. The effect of frontal
8. Koval R, Teller J, Belkin M, et al. The Israeli ocular injuries
airbags on eye injury patterns in automobile crashes. Arch
study, a nationwide collaborative study. Arch Ophthalmol
Ophthalmol 2002;120:1517–1522.
1988;106:776–780.
23. Anderson SK, Desai UR, Raman SV. Incidence of ocular injuries
9. Dandona L, Dandona R, Srinivas M, et al. Ocular trauma in an
in motor vehicle crash victims with concomitant air bag
urban population in southern India: the Andhra Pradesh Eye
deployment. Ophthalmology 2002;109:2356–2358.
Disease Study. Clin Exp Ophthalmol 2000;28:350–356.
24. Lehto KS, Sulander PO, Tervo TM. Do motor vehicle airbags
10. Moreira CA, Debert-Ribeiro M, Belfort R. Epidemiological
increase risk of ocular injuries in adults? Ophthalmology
study of eye injuries in Brazilian children. Arch Ophthalmol
2003;110:1082–1088.
1988;106:781–784.
25. McGwin G, Owsley C. Risk factors for motor vehicle collision-
11. Dannenberg AL, Parver LM, Brechner RJ, Khoo L. Penetrating
related eye injuries. Arch Ophthalmol 2005;123:89–95.
eye injuries in the workplace, the national eye trauma system
26. Schein OD, Hibberd PL, Shingleton BJ, et al. The spectrum
registry. Arch Ophthalmol 1992;110:843–848.
and burden of ocular injury. Ophthalmology
12. Yu TSI, Liu H, Hui K. A case-control study of eye injuries in the
1988;95:300–305.
workplace in Hong Kong. Ophthalmology 2004;111:70–74.
27. Baker RS, Wilson MR, Flowers CW, et al. A population-based
13. Voon LW, See J, Wong TY. The epidemiology of ocular trauma
survey of hospitalized work-related ocular injury: diagnoses,
in Singapore: perspective from the emergency service of a
cause of injury, resource utilization, and hospitalization
large tertiary hospital. Eye 2001;15:75–81.
outcome. Ophthalmic Epidemiol 1999;6:159–169.
5
2
Prevention of eye injuries
Paul M. Gallogly, Stephanie L. Vanderveldt, James T. Banta
INTRODUCTION A number of professional organizations are

involved in the standards of eye protection
The vast majority of eye injuries are preventable manufacturing, testing of eyewear to conform
with currently available protective devices. to safety standards, and dissemination of safety
Nevertheless, nearly 55 million eye injuries that information to educate the public. They
restrict activities for more than 1 day occur each include:
year.1 As eye care professionals we must identify 1. ANSI: The American National Standards
and educate those individuals at risk for ocular Institute is an organization which facilitates
injury. voluntary consensus standards in the US and
The initial step in preventing ocular injury is abroad. ANSI is a private, nonprofit organiza-
identifying patients at risk. One may argue that tion that promotes voluntary consensus stan-
the entire population carries some inherent risk. dards including standards for eye protection,
This of course is true, but identification of both personal and occupational. ANSI pro-
patients with high-risk jobs or activities may vides standards for the strength of polycar-
help limit preventable ocular trauma. A simple bonate lenses and the manufacture and design
history of daily activities and hobbies obtained of safety spectacle frames and chemical
by the ophthalmologist or technician can quickly eyewash stations, among many other safety
and easily identify these patients. Brief questions standards. More information is available at
may include: ‘What are your hobbies?’ ‘Are you www.ANSI.org.
involved in sports activities?’ ‘What is your 2. ASTM: ASTM International, formerly the
occupation?’ A previous history of ocular trauma American Society for Testing and Materials,
is equally important, as studies have shown that is a voluntary standards development organi-
ocular trauma is a recurrent disease.2 zation generating standards for the manufac-
Another important population that must be turing of a wide variety of materials including
identified is the patient with one functional eye. sports eye protectors. ASTM International
The functionally one-eyed patient is an individ- certifies racket sport eye protectors as well as
ual who would have a significant change in life- those for paintball, baseball, downhill skiing,
style if the better-seeing eye was damaged or and ice hockey. The ASTM standards for
lost. Some common examples include patients racket sport wear are significantly more strin-
with amblyopia, decreased vision due to a prior gent than those of ANSI. More information is
traumatic event, or decreased vision due to a available at www.ASTM.org.
chronic but asymmetric ocular condition (e.g. 3. PECC: The Protective Eyewear Certification
glaucoma). After the ophthalmologist has appro- Council independently tests and certifies
priately identified those individuals with preven- eyewear in hopes of reducing eye injuries.
tative needs, recommendations must be given in Manufacturers that produce products passing
a simple and directed manner. their standards bear the seal of the
7
Ocular trauma
organization. More information is available at organization works to educate the public

www.PROTECTEYES.com. about ocular public health issues, including
4. CSA: The Canadian Standards Association prevention of ocular injuries. More informa-
works to develop standards for a multitude of tion is available at www.AAO.org.
items, particularly items meant to enhance Given the sheer number of high-risk activities,
public safety. They also work to educate the the scope of this chapter does not allow the
public about these standards. More informa- authors to cover each activity in detail. Special
tion is available at www.CSA.ca. mention will be given to a few high-risk situa-
5. HECC: The Hockey Equipment Certification tions that are most frequently associated with
Council independently reviews the recom- eye injuries, namely: work, sport, driving, and
mendations of various hockey organizations assault.
with regard to safety equipment and certifies
specific safety products by validating the LENS MATERIALS
testing performed by the manufacturer. This
organization is supported by USA Hockey Glass or allyl resin plastic (CR-39) lenses, present
who require the use of HECC-certified equip- in nearly 90% of all dispensed spectacles, have
ment in official play. HECC refers to ASTM little impact resistance, are prone to shatter, and
F513 guidelines in certification testing of all have caused eye injury as a result of this shatter-
eye and face protectors. More information is ing. The material of choice for all protective
available at www.HECC.net. lenses, both street-wear and active-wear, is poly-
6. NOCSAE: The National Operating Commit- carbonate. Polycarbonate lenses have excellent
tee on Standards for Athletic Equipment is impact resistance, good optical properties, and
involved in testing and implementing test acceptable UV absorption. They are thinner,
standards for various sports in a concerted lighter, equally scratch resistant, and significantly
effort to reduce injuries. More information is safer than glass or CR-39 plastic lenses.
available at www.NOCSAE.org. Polycarbonate lenses are not without limita-
7. OSHA: The Occupational Safety and Health tions, however. First, there is a cost differential
Administration is a component of the US of approximately $25 for polycarbonate lenses
Department of Labor that establishes stan- vs. CR-39. Additionally, there is a limitation in
dards to ensure the safety and well-being of the range of refractive errors that can be accom-
American workers. In particular, OSHA modated. Most companies can accommodate
governs the requirements for use and mainte- refractive errors of 12–14 diopters of myopia.
nance of occupational eye protection in various Recently, with refi nements of high-index poly-
industrial settings. The organization also pro- carbonate, prescriptions can be fi lled up to 20
vides employee training requirements for the diopters of myopia, albeit at a premium cost.
use of protective equipment and the care, Chromatic aberration at the lens periphery of
maintenance, and inspection of such equip- high minus polycarbonate lenses is also encoun-
ment. More information is available at www. tered. Athletes or workers with a large refractive
OSHA.gov. error that precludes the use of polycarbonate
8. AAO: The American Academy of Ophth- should wear contact lenses with the appro-
almology is the professional society of priate non-prescription polycarbonate protective
ophthalmologists in the United States. The device.
8
WORK-RELATED INJURIES
In industrialized countries, approximately 14%

of all ocular injuries take place within the work-
place. The direct cost of these ocular injuries is
estimated to be more than $500 million annu-
ally. 3 In many instances, ‘safety’ eyewear is inade-
quate or simply not worn. A study of open globe
injuries in workers in the United States showed
that only 6% of workers were wearing eye pro-
tection at the time of injury.4 These numbers
leave tremendous room for improvement, as the
use of appropriate protective devices can prevent
most, if not all of these injuries.
Specific occupations inherently carry more
risk. As elicited in the 1994 Bureau of Labor
Statistics,5 the risk of ocular injury is as
follows:
1. Construction: 29 per 10 000 Figure 2.1 Industrial eye protectors should meet or
exceed ANSI Z87.1 and when feasible should include
2. Agriculture, fi shing, and forestry: 25 per
side shields. Protectors are available that fit over
10 000
prescription eyewear. (Photo courtesy of Miller Electric
3. Manufacturing: 17 per 10 000 Manufacturing Company.)
4. Mining: 13 per 10 000.
In the case of work-related injuries, the eye care
professional must go beyond the injured employee
and involve company management in prevention falling objects smaller than the head of a pin. In
strategies. Appropriate eyewear must be made general, ANSI Z87.1 is the standard to which
available, and consequences for not wearing industrial eye protectors should be held. Safety
appropriate eye protection must be instituted. spectacles with side shields are the minimum
This multilevel approach provides the greatest protective equipment required when working in
potential for improved eye safety in the an area with a potential impact hazard (Figure
workplace. 2.1). Clinically, many injuries are seen from
objects flying under the rim of safety spectacles,
Industrial eye protectors particular with grinding and hammering. There-
Industrial eye injuries are responsible for the vast fore, polycarbonate goggles should be considered
majority of metallic corneal foreign bodies, and standard protection for workers exposed to high
more seriously, intraocular foreign bodies. In velocity or large fragments (Figure 2.2). If the
particular, hammering metal on metal and grind- occupation poses additional hazard to the face,
ing are two common causes of injury. According a face shield should be employed. Since face
to the US Department of Labor Occupational shields are often lifted in the midst of work
Safety and Health Administration (OSHA), the activities, it is recommended that safety glasses
majority of impact injuries result from flying or with side shields be worn under the shield.
9
Ocular trauma
Figure 2.3 Welding masks that meet or exceed ANSI

Z49.1 should be used over goggles or safety spectacles
with side shields. (Photo courtesy of Miller Electric
Manufacturing Company.)
splash, irritating mists, vapors, and fumes. OSHA

Figure 2.2 Polycarbonate goggles should be recommends that face shields should be used as
considered standard protection when high-velocity secondary protectors to shield the entire face
impact potential exists. (Photo courtesy of Miller from exposure to chemical hazards. For work-
Electric Manufacturing Company.)
places that pose a dust hazard, safety goggles are
recommended and the use of contact lenses is
OSHA requires workers who are exposed to discouraged.
high temperatures, splashes from molten metal, Finally, optical radiation is a risk in work
or sparks (those involved in pouring, casting, hot environments with exposure to intense heat,
dipping, furnace operations, or welding) to use ultraviolet, infrared, or reflected light radiation.
goggles or special-purpose lenses in appropriate Welders and workers exposed to lasers fall into
safety spectacles with side shields. Protective this category. The lens and glare requirements
devices for welding are held to the higher ANSI for adequate protection in these scenarios are
Z49.1 standard which requires the use of safety based on the maximum power density that the
spectacles with side shields or goggles to be worn lasers produce.
underneath a facemask fitted with a fi ltered
safety lens (Figure 2.3). Chemical eyewash stations
With regard to chemical hazards, goggles are Eyewash stations are required by OSHA to be
the primary means of protection against liquid placed in any location where there is a reasonable
10
probability of injury that may require treatment.

Table 2.1 Risk categories for sports-related
Laboratories in which corrosive or biohazardous eye injury for the unprotected player.
chemicals are present are a common example.
OSHA requires that these chemical eyewash sta- High risk
tions follow ANSI Z358.1 standards. In general, Small, fast projectiles
–Air rifle/BB gun
eyewash stations are designed to provide a steady
–Paintball
soft stream of water (15–35° Celsius) not less
Hard projectiles, fingers, ‘sticks,’ close contact
than 11.4 L per minute for at least 15 minutes. –Baseball/softball/cricket
The station is manufactured to provide continu- –Basketball
ous irrigation simultaneously to both eyes while –Fencing
the user manually opens and holds the eyelids. –Field hockey
–Ice hockey
On–off valves on eyewash stations must be acti-
–Lacrosse, men’s and women’s
vated in 1 second or less and must remain on
–Squash/racquetball
without the use of the operator’s hands until –Street hockey
intentionally discontinued. The eyewash stations Intentional injury
are to be inspected monthly to assure that they –Boxing
are in proper working order and are freely –Full-contact martial arts
accessible. Moderate risk
Fishing
SPORTS INJURIES Football
Soccer/volleyball
Tennis/badminton
Almost every type of sport has been associated
Water polo
with eye injury. In the United States alone, an
Low risk
estimated 40 000 sports- and recreation-related
Bicycling
eye injuries were reported in 2000. The eye
Noncontact martial arts
injury risk of a sport is proportional to the likeli- Skiing
hood of the eye being impacted with sufficient Swimming/diving/water-skiing
energy to cause harm. Vinger et al categorized Wrestling
common sports into four types: high risk, Eye safe
moderate risk, low risk, and eye safe (Table 2.1).6 Gymnastics
Among individuals older than 5 years of age, the Track and field*
two sports most commonly associated with eye *Javelin and discus have a small but definite
injuries were basketball and baseball. potential for injury that is preventable with good
The sport of hockey is a good example of posi- field supervision.
tive results from preventative measures. In the (From Vinger PF. A practical guide for sports eye
protection. Physician and Sports Medicine
1977–78 season, the National Collegiate Athletic
2000;28(6):49–69, with permission.)
Association (NCAA) required full facemasks to
be worn in all college hockey games in the United
States.7 As seen in Figure 2.4, eye injuries have
fallen sharply since the introduction of new rules
and use of facemasks. A study of junior hockey
11
Ocular trauma
300 50
Total 45
250 Introduction of new rules
Blinding
40
Total number of eye injuries
Number of blinding injuries

200 35
Mandatory use 30
150 of face mask 25
20
100
15
10
50
5
0 0
1972–73
1974–75
1976–77
1977–78
1978–79
1979–80
1980–81
1981–82
1982–83
1983–84
1984–85
1985–86
1986–87
1987–88
1988–89
1989–90
1990–91
1991–92
1992–93
1993–94
1994–95
1995–96
1996–97
1997–98
1998–99
1999–00
2000–01
Figure 2.4 Canadian Ophthalmological Society survey of eye injuries from 1972 to 2002. The introduction of high
sticking and hooking penalties in 1975 and the mandatory use of certified full facemasks in 1978 are indicated.
(From Biasca N, Wirth S, Tegner Y. The avoidability of head and neck injuries in ice hockey: an historical review. Br J
Sports Med 2002;36(6):410–427, with permission from BMJ Publishing Group.)
players aged between 16 and 21 years found that devices for each activity. In a joint policy state-
the risk of eye injury was 4.7 times greater for ment by the American Academies of Pediatrics
players wearing no facial protection than for and Ophthalmology, specific recommendations
those wearing partial facial protection.8 Some for various sporting activities were created
debate remains as to which is more appropriate (Table 2.2). 9 This provides a handy reference in
overall, full facemasks or helmets with a visor; the office or can be given to patients as reference
but there is no question that some form of pro- material.
tection reduces ocular injuries. Protective eyewear for leisure and sports fall
Ideally, any patient participating in an ‘at-risk’ into three main categories:
sport should wear protective devices. Recom- 1. Street-wear frames with 2 mm polycarbonate
mendations for eyewear protection should be lenses. This combination is generally accept-
individualized for each patient. Collaboration able for everyday use by functionally one-eyed
with managers of community sports leagues and patients and active people in low eye risk
schools will also increase awareness of the need activities (sports not involving a thrown or hit
for eye protection. ball, the use of a bat or stick, or close aggres-
sive play with body contact).10 They may also
Eye protection for leisure and sports be acceptable for use under a facemask in
The eye professional must have a working knowl- hockey, football, or lacrosse. It is, however,
edge of the various types of eye protection. Many generally considered inadequate protection
patients will require more than one protective for the functionally one-eyed patient to use
device for differing occupational and leisure sce- street-wear frames under a facemask. A racket
narios. For instance, a welder who plays racquet- sport eye protector is advised for tennis and
ball for fitness will need different protective other racket sports.11
12
Table 2.2 Recommended eye protectors for selected sports.
Sport Minimal eye protector Comment

Baseball/softball (youth ASTM F910 Faceguard attached to helmet
batter and base runner)
Baseball/softball (fielder) ASTM F803 for baseball ASTM specifies age ranges
Basketball ASTM F803 for basketball ASTM specifies age ranges
Bicycling Helmet plus street-wear/fashion
eyewear
Boxing None available; not permitted Contraindicated for functionally
in sport one-eyed athletes
Fencing Protector with neck bib
Field hockey (men and women) ASTM F803 for women’s lacrosse Protectors that pass for women’s
Goalie full facemask lacrosse also pass for field hockey
Football Polycarbonate eye shield attached
to helmet-mounted wire facemask
Full-contact martial arts None available; not permitted Contraindicated for functionally
in sport one-eyed athletes
Ice hockey ASTM F513 facemask on helmet; HECC or CSA certified;
Goaltenders ASTM F1587 Full-face shield
Lacrosse (men) Facemask attached to lacrosse
helmet
Lacrosse (women) ASTM F803 for women’s lacrosse Should have option to wear helmet
Paintball ASTM F1776 for paintball
Racket sports (badminton, ASTM F803 for selected sport
tennis, paddle tennis,
handball, squash, and
racquetball)
Soccer ASTM F803 for selected sport
Street hockey ASTM 513 face mask on helmet Must be HECC or CSA certified
Track and field Street-wear with polycarbonate
lenses/fashion eyewear*
Water polo/swimming Swim goggles with polycarbonate
lenses
Wrestling No standard available Custom protective eyewear can be
made
*Eyewear that passes ASTM F803 is safer than street-wear eyewear for all sports activities with impact
potential.
(From American Academy of Pediatrics, Committee on Sports Medicine and Fitness. American Academy of
Ophthalmology, Eye Health and Public Information Task Force. Protective eyewear for young athletes.
Ophthalmology 2004;111(3):600–603, with permission from the American Academy of Ophthalmology.)
13
Ocular trauma
eye protectors when involved in high eye risk

activities.
3. Helmet–facemask combinations. Helmet–
facemask combinations are suggested for
extremely high eye risk activities and sports
such as hockey, football, lacrosse, baseball,
downhill skiing, fencing, and motocross.
These are examples of activities for which
ASTM standard F803 protection is consid-
ered inadequate. As previously discussed,
the regulated use of helmet–facemask com-
binations in the sport of hockey has all but
eliminated eye injury. Fineman et al, while
investigating a series of paintball-associated
ocular traumas, noted that none of the injured
subjects were wearing eye protective devices
that met current ASTM standards.13 Specific
ASTM standards for many sports can be found
in the appendix at the end of this chapter.
Additional standards are available for youth
Figure 2.5 Polycarbonate sports goggles that meet or baseball/softball batter and catcher face
exceed ASTM F803 should be used for all high-risk shields, football helmets, lacrosse helmets
sporting activities, particularly racket sports. Many with faceguards, polo helmet-mounted eye
models can have prescription lenses fitted. (Photo
protection, and hockey face protectors and
courtesy of Hilco.)
helmets through the National Operating
Committee on Standards for Athletic Equip-
2. Sports frames with 3 mm polycarbonate lenses. ment (www.NOCSAE.org).
Frames which meet ASTM standard F803 cri- Functionally one-eyed patients should be dis-
teria are required for use by persons engaged couraged from participating in very high eye risk
in high eye risk activities and non-collision sports such as boxing, full-contact martial arts,
sports (racket sports, baseball fielders, basket- and wrestling. These activities not only pose
ball, soccer) and for all functionally one-eyed extreme danger to the eyes, but also do not allow
patients engaged in any sporting activity for the reduction of risk by the use of protective
(Figure 2.5).12 Although ASTM criteria are devices.
specifically applied to eye protectors for racket
sports, it is generally recommended that these Paintball
be used for other non-collision sports as Paintball is a relatively new sport in which par-
well. There are presently no standards for ticipants play various war games using guns to
non-collision sports such as soccer and basket- shoot opponents with small paint-fi lled projec-
ball. Sports participants without refractive tiles. The compressed air or gas rifles used in the
error or who wear contact lenses should sport have a muzzle velocity of 80–130 m/sec.14
wear non-prescription polycarbonate sports In the United States, participation in paintball
14
has increased in popularity tenfold since 1989.15

There were approximately 6.4 million partici-
pants in 2000 with increasing numbers yearly.16
With the increase in popularity has come an
increase in ocular injuries. A large increase in
ocular injuries secondary to paintball and related
war games is presently being encountered in
emergency rooms in many countries, and it is
this rash of severe ocular injuries which warrants
special mention. The incidence of paintball eye
injuries treated in emergency departments in the Figure 2.6 Eye protection for paintball-related
United States rose from an estimated 545 in activities should meet or exceed ASTM F1776. (Photo
courtesy of Draxxus/VForce Paintball.)
1998 to more than 1200 in 2000.17
Since 1985, visual acuity less than or equal to
20/400 was reported in 37% of reported paint-
ball injuries. Most, if not all of these injuries paintball that meet or exceed ASTM F1776 are
could have been prevented by the use of proper utilized (Figure 2.6).
eye protection. In a recent series, 63% of players
were using eye protection prior to the time of
injury; unfortunately 86% removed this eye pro- AIRBAG INJURIES
tection immediately prior to injury.13 Profes-
sional paintball tournaments and commercial In the United States the use of both driver and
venues have stringent, enforced safety require- passenger side airbags in conjunction with three-
ments. In these settings, paintball can be a rela- point lap restraints was mandated in 1997.
tively safe activity. However, players sometimes Deployment of an airbag occurs in three steps.
remove their protection because they are not In the fi rst step sensors detect a crash. This
involved in the active game or they feel the pro- results in rapid oxidation of a propellant that
tection is too warm to wear. There is also a trend inflates the bag at a velocity of 100–200 mph.
away from commercial vendors and towards non- Talc is used in the packaging of the airbag and is
commercial and private use of paintball devices. also released in the process. Gases are vented to
Such a trend may suggest an increase in the use partially deflate the airbag, softening the occu-
of paintball weapons in unsupervised locations pant’s ‘landing.’ According to statistics on frontal
without proper protective devices. Parents need crashes from the US Department of Transporta-
to be informed of the inherent dangers of paint- tion, airbags are estimated to reduce the number
ball equipment and should keep it locked away of fatal injuries by 31–32% above and beyond the
as they would any fi rearm, allowing it to be used 45% reduction afforded by seatbelts.18
only in organized and supervised settings. Although airbags can significantly reduce mor-
Although ASTM does not specifically test tality, they also are associated with serious eye
paintball goggles, it did release a voluntary injury. There is a broad spectrum of eye injuries
standard for paintball goggle testing (ASTM associated with airbags including, but not limited
F1776-01). When advising a patient, make to, burns, lacerations, corneal abrasions, hyphe-
certain that goggles developed specifically for mas, retinal detachments, and ruptured globes.
15
Ocular trauma
Long-term visual outcome data is not available because information on the use of eyeglasses was
because the literature consists largely of case not provided at the time of data collection.20
reports and small case series. The authors are of The only realistic strategy to reduce assault-
the opinion that the life-preserving function of related eye injuries is violence prevention. If
airbags far outweighs the risk of eye injury. abuse or violence is suspected, directed ques-
Research and development by car companies and tions regarding abusive or violent situations
engineers aimed at increasing the safety profi le should be posed. When appropriate, law enforce-
of airbags while maintaining their life-preserving ment and social services should be utilized in
function is ongoing. Newer, ‘depowered’ airbags hopes of preventing further violence. Legal
are now standard on all cars produced after 1997 requirements vary, but most states have manda-
and have recently been reported to lessen the tory reporting requirements when abuse is sus-
risk of eye injury.19 pected, particularly when children and the
elderly are involved.
ASSAULT-RELATED INJURIES
Violence is a significant cause of ocular trauma. CONCLUSION

In 1992, assault accounted for more than 20% of
the penetrating eye injuries reported to the Prevention of eye injuries receives little of the
National Eye Trauma System Registry. A review attention it deserves. Modifying risk factors and
of the literature suggests that assault-related implementing appropriate eyewear protection
injuries involve primarily young males, together strategies can reduce the rates of ocular injury
with alcohol or drugs, unsettled social environ- while allowing patients to maintain a productive
ments, and unemployment. As reported by career and enjoy their leisure time to the fullest.
Dannenberg et al, a wide variety of objects are It is the duty of the eye care professional to be
used as weapons in assaults. The most common familiar with the many safety devices and ask
object used was the fi st. The protective value of directed questions to help best protect the
spectacles could not be assessed in this report patient.
16
Appendix: Eye protection standards and guidelines
Nonsporting activities
American National Standards Institute:
ANSI Z80.1 Requirements for first quality prescription ophthalmic lenses

ANSI Z80.3 Nonprescription sunglasses and fashion eyewear
ANSI Z80.5 Prescription ophthalmic frames
Recreation, hobbies, occupation
American National Standards Institute:
ANSI Z87.1 Practice for occupational eye and face protection

ANSI Z49.1 Safety in welding, cutting, and allied processes
Sports
American Society for Testing and Materials:
ASTM F803-03 Eye protectors for selected sports (racket sports, women’s lacrosse, baseball,
field hockey)
ASTM F513-00 Eye and face protective equipment for hockey players
ASTM F659-98e1 Skier goggles and face shields
ASTM F1776-01 Eye protector for use by players of paintball sports
ASTM F910-04 Face guards for youth baseball
ASTM F1587-99 Head and face protective equipment for ice hockey goaltenders
For sports with no standard (basketball, soccer, rugby) a minimal eye protector requirement
should be ASTM F803.
17
Ocular trauma
REFERENCES 10. International Federations of Sports Medicine. Position

statement: eye injuries and eye protection in sports.
Physician and Sports Medicine 1988;16(11):49–51.
1. Negrel AD, Thylefors B. The global impact of eye injuries.
11. Vinger PF, Tolpin DW. Racquet sports: an ocular hazard.
Ophthalmic Epidemiol 1998;5(3):143–169.
JAMA 1978;239:2575–2577.
2. Wong TY, Klein BE, Klein R. The prevalence and 5-year
12. Easterbrook M. Ocular injuries in racquet sports. Int
incidence of ocular trauma: Beaver Dam Eye Study.
Ophthalmol Clin 1988;28:232–237.
Ophthalmology 2000;107:2196–2202.
13. Fineman MS, Fischer DH, Jeffers JB, Buerger DG, Repke C.
3. Baker RS, Wilson MR, Flowers CW, Lee DA, Wheeler NC.
Changing trends in paintball sport-related ocular injuries.
Demographic factors in population-based survey of
Arch Ophthalmol 2000;118:60–64.
hospitalized, work-related, ocular injury. Am J Ophthalmol
14. Zwaan J, Bybee L, Casey P. Eye injuries during training
1996;122:213–219.
exercises with paint balls. Mil Med 1989;161:720–722.
4. Dannenberg AL, Parver LM, Brechner RJ, Khoo L. Penetrating
15. Kitchens JW, Danis RP. Increasing paintball related eye trauma
eye injuries in the workplace, the National Eye Trauma System
reported to a state eye injury registry. Injury Prevention
Registry. Arch Ophthalmol 1992;110:843–848.
1999;5(4):301–302.
5. US Bureau of Labor. Work injuries and illnesses by selected
16. Capao-Filipe JA, Rocha-Sousa A, Falcao-Reis F, Castro-Correia
characteristics. Washington, DC: US Bureau of Labor, 1994.
J. Modern sports eye injuries. Br J Ophthalmol 2003;87(11):
6. Vinger PF. A practical guide for sports eye protection.
1336–1339.
Physician and Sports Medicine 2000;28(6):49–69.
17. Listman DA. Paintball injuries in children: more than meets
7. Biasca N, Wirth S, Tegner Y. The avoidability of head and neck
the eye. Pediatrics 2004;113(1):e15–18.
injuries in ice hockey: an historical review. Br J Sports Med
18. Pearlman JA, Au Eong KG, Kuhn F, Pieramici DJ. Airbags and
2002;36(6):410–427.
eye injuries: epidemiology, spectrum of injury, and analysis of
8. Stuart MJ, Smith AM, Malo-Ortiguera SA, et al. A comparison
risk factors. Surv Ophthalmol 2001;46(3):234–242.
of facial protection and the incidence of head, neck and
19. Duma SM, Rath AL, Jernigan MV, Stitzel JD, Herring IP. The
facial injuries in Junior A hockey players: a function of
effects of depowered airbags on eye injuries in frontal
individual playing time. Am J Sports Med 2002;30:39–44.
automobile crashes. Am J Emergency Med 2005;23:13–19.
9. American Academy of Pediatrics, Committee on Sports
20. Dannenberg AL, Parver LM, Fowler CJ. Penetrating eye
Medicine and Fitness, American Academy of Ophthalmology,
injuries related to assault: the National Eye Trauma System
Eye Health and Public Information Task Force. Protective
Registry. Arch Ophthalmol 1992;110:849–852.
eyewear for young athletes: joint policy statement.
Ophthalmology 2004;111:600–603.
18
3
History and examination of
the injured eye
Alexei L. Moraczewski
GENERAL MEDICAL EVALUATION1,2 other symptoms such as pain, diplopia, and

photophobia.
In many cases involving ocular trauma, the oph- The details of the traumatic incident should be
thalmologist is the fi rst physician to assess the recorded:
patient. Many patients with ocular trauma also 1. Date, time and location of the incident
sustain non-ocular trauma as well; thus it is 2. Mechanism of injury (struck by fi st, hammer-
crucial to ensure that life-threatening injuries ing metal on metal, etc.)
are not present before focusing attention on the 3. Accidental, intentional, or self-infl icted
eye. The initial assessment of the traumatized injury
patient should include measuring vital signs and 4. Accident setting (work, home, sports-related,
mental status as well as a rapid general physical etc.)
examination to exclude any soft tissue or bony 5. Use of contact lenses, corrective glasses, or
injuries. If conditions such as respiratory dis- safety glasses at the time of accident
tress, cardiovascular instability, massive bleed- 6. Presence of witnesses to the accident.
ing, or an acutely impaired mental status are The mechanism of injury is particularly useful
encountered, the patient should be transferred for determining the level of suspicion for intra-
immediately to an emergency room or trauma ocular or intraorbital foreign bodies.
center. In cases of mechanical trauma to the eye with
Once the general medical stability of the a foreign object, it is important to note:
patient is ensured, a general medical history 1. The physical characteristics of the object
should be obtained to document all current and causing the trauma (e.g. size, presence of
past medical conditions, previous surgeries, sharp edges)
current medications, known drug allergies, use 2. The distance and direction traveled to the
of alcohol and illicit drugs, and tetanus immuni- eye
zation status. 3. The location of the impact
4. The condition of any eyewear used at the time
HISTORY1,3 of injury.
An initially high level of suspicion for intraocular
A focused yet careful history is important, as it or intraorbital foreign bodies should be main-
often plays a large role in guiding further evalu- tained with any ocular trauma. In highly sus-
ation and management. The history should be pected or confi rmed cases of foreign bodies, the
well documented in the medical record, espe- following information should be gathered:
cially given the increased incidence of litigation 1. The composition of the foreign body (which
following ocular trauma. The patient should be determines its ocular toxicity)
questioned about any sudden or gradual changes 2. The origin of the foreign body (fragment from
in vision since the time of the trauma, as well as a metal tool, glass from a windshield)
19
Ocular trauma
3. Activity at the time of the injury 3. The animal should be located to allow testing
4. The possibility of single or multiple foreign for the presence of transmissible disease, if
bodies necessary.
5. The distance, direction, and speed traveled by A brief, directed past ocular history should
the foreign body include pre-existing ocular conditions, prior
6. The position of the patient’s head and direc- ocular surgeries, and level of vision prior to the
tion of gaze at impact trauma. Previous ocular surgery can increase sus-
7. A description and the composition of tools, ceptibility to traumatic injury. The presence of
machinery, grinding surfaces, or weapon used intraocular (e.g. intraocular lens) or periocular
at the time of the injury appliances (e.g. scleral buckle, glaucoma drain-
8. Possible contamination of foreign bodies age implant) should be noted. Any previous
with oil, grease, dirt, or vegetable matter treatment for the injury should be recorded, in-
(to determine the risk of microbiologic cluding self-administered treatment. The routes,
contamination). dosages, and timing of any administered medica-
Chemical injuries, especially with alkali sub- tions should be recorded. The names, locations,
stances, are true ophthalmic emergencies, and and phone numbers of any physicians who previ-
immediate irrigation should be initiated prior to ously treated the patient should be recorded in
obtaining a detailed history. Once initial treat- the event that they need to be contacted about
ment has been administered, the following the case.
should be performed:
1. The chemical (acid or alkali) and physical
(liquid, gel, particulate) properties of the sub- EXAMINATION
stance should be established.
2. The pH of the substance should be measured General considerations
if a sample is available. The examination of an injured eye is fraught
If the identity or characteristics of the substance with difficulty. The anxiety and pain of the
are unusual or unknown, the local poison control patient with a potentially vision-threatening
center can be extremely helpful in providing this injury often makes for a less than desirable
information. cooperative effort. It is vital to establish a rapport
In the uncommon cases of thermal burns, with the patient and family and quickly lay the
the type and temperature of the involved mate- foundation for effective communication and
rial and duration of contact should be elicited. trust. Simply acknowledging the obvious anxiety
If the trauma involves electrical burns, the and potential concern of the patient can do much
amount of electrical energy involved and the to alleviate anxiety and allow proper examina-
entrance and exit points should be determined tion. Furthermore, during the examination,
if possible. explaining each step can help calm the patient.
Following injuries from animals: In the setting of a potential open globe injury,
1. The type of animal and how the injury was everything must be done to expedite the history
infl icted (e.g. bite, scratch) should be and examination process while minimizing
identified. manipulation of the eye. We routinely put a
2. It should be determined if the attack was metal shield over injured eyes before taking any
spontaneous or provoked. history to prevent the patient from touching or
20
History and examination of the injured eye
specific scenarios in which they add to the diag-

nostic work-up. Although the following pages
describe examination techniques in great detail,
complete yet efficient examinations can mini-
mize patient anxiety, expedite the patient’s
work-up, and lead to a more rapid resolution of
the patient’s problem.
Visual acuity1,2,4
The aims of visual acuity testing are to deter-
mine an estimate of the patient’s visual function
and establish a baseline to which future exami-
nations can be compared. Visual acuity is often
an important prognostic indicator of fi nal visual
Figure 3.1 Desmarres retractors are used to gently function following trauma.
open the eyelids of a patient with orbital compartment Ideally, the visual acuity should be measured
syndrome.
in each eye separately using a standard Snellen
visual acuity chart. The patient’s corrective
rubbing the eye. Examination should be carried glasses should be used if available. If the patient’s
out only by those specifically trained to care for glasses are not available or the patient’s refractive
ocular emergencies. error is unknown, pinhole acuity should be mea-
Extensive periorbital swelling and hemorrhage sured. If a standardized distance vision chart is
are often encountered in the acute setting. If the not available, a near vision card or representative
patient is unable to open the injured eye, the use newsprint can be substituted. Correction of
of Desmarres eyelid retractors is sometimes nec- presbyopia may be required depending on the
essary (Figure 3.1). These retractors are designed age and refractive status of the patient. The
to minimize anterior–posterior pressure on the method used to check visual acuity should be
eye while allowing access to the injured eye. documented in the medical record.
Included
on DVD
Depending on the extent of periocular swelling, When the vision is too poor to be measured
the examiner can sometimes hold a single retrac- with a vision chart, a gross assessment of vision
tor under the upper lid and proceed with the is documented (counting fi ngers at a specified
examination one-handed. However, it is some- distance, hand motions, light perception with
times more convenient to have a second trained or without projection, no light perception). If
staff member hold the eyelid retractors so the the patient is found to have no light perception,
physician is free to use both hands. this should be confi rmed and recorded by the
Finally, common sense must be emphasized. physician using the brightest light source
Certain examination steps are sometimes de- available (usually an indirect ophthalmoscope)
ferred in the acute setting. Intraocular pressure while occluding the uninvolved eye completely.
is not checked until the structural integrity of
the eye is confi rmed. Scleral depression, color Pupils1,3,4
vision testing, and forced ductions are not neces- Examination of the pupils provides valuable
sary on every patient and should be reserved for information about potential damage to the visual
21
Ocular trauma
system as well as possible intracranial pathology. Baseline
The pupils may provide the only information

about the visual system if the patient is not
conscious. The pupils should be examined for a
direct and consensual response to light. A poorly Dim illimination Left eye obscured or
maintained on right pupil previously dilated
responsive, dilated pupil is usually the result of
direct trauma to the eye that leads to traumatic Normal response
mydriasis or iris sphincter damage; pharmaco-
logic dilation must also be considered, particu- Constriction
larly if the patient has been transferred from
another emergency room or physician. In cases Bright illumination
No RAPD
of head trauma, however, a fi xed dilated pupil
can signify compression of the third cranial nerve
from increased intracranial pressure from sources Constriction
such as epidural or subdural hematomas. A fi xed

dilated pupil can also be a sign of direct injury Bright illumination
to the third cranial nerve, its nucleus, or the

ciliary ganglion.
Abnormal response
The presence of a relative afferent pupillary
defect (RAPD) indicates dysfunction of the
Constriction
afferent visual pathway. After focal ocular
trauma, an RAPD is typically a result of damage
Bright illumination
to the optic nerve (e.g. traumatic optic neuropa- RAPD by reverse
thy) or diffuse retinal injury (e.g. retinal detach-

ment). Very rarely will opacities of the media
Dilation
(e.g. cataract, hyphema, vitreous hemorrhage)
cause an RAPD. An RAPD is detected utilizing Bright illumination
the swinging flashlight test, where a light source
is rhythmically shifted back and forth from one Figure 3.2 Testing for a relative afferent pupillary defect
pupil to the other. An RAPD is present in a pupil when one pupil is obscured or dilated requires
continuous, mild illumination of the normal uninvolved
that paradoxically dilates when the light is shone
pupil. We often use the light from a direct
into it. The swinging flashlight test can be used
ophthalmoscope turned down to a setting where the
even if one pupil is obscured, severely damaged, uninvolved pupil is just visible. A second bright light
or pharmacologically dilated. Using a separate source is used to test each pupil individually. We typically
light source to illuminate the uninvolved pupil, use an indirect ophthalmoscope turned up to its
the test is performed normally, but only the maximum intensity for this purpose. The light source is
swung rhythmically between the two pupils and the
response of the uninjured or undilated pupil is
response of the uninvolved pupil is noted. In the absence
monitored. If an RAPD is present in the injured
of an RAPD, the uninvolved pupil should constrict when
eye, the reactive uninjured eye will consensually the bright light source is introduced to either eye. An
dilate when the light is directed toward the ‘RAPD by reverse’ is present when the uninvolved pupil
injured eye (Figure 3.2). This is sometimes paradoxically dilates when the light source is introduced
referred to as an ‘RAPD by reverse.’ to the involved pupil, denoting injury to the anterior
visual pathway (typically the optic nerve).
22
The shape of the pupil should be noted. An acuity is poor or optic nerve dysfunction is
eccentric or peaked pupil may indicate a trau- suspected.
matic iridodialysis, iris sphincter tear, vitreous Formal visual field testing (e.g. static auto-
prolapse into the anterior chamber or an open mated perimetry or Goldmann perimetry)
globe injury with iris prolapse. usually can be deferred in the emergency setting
unless it is needed for diagnostic purposes.
Brightness testing and color vision2,4 This requires that the patient is stable, coopera-
Brightness testing is a quick subjective test of tive, and can sit upright. Formal visual field
optic nerve function. A bright light source is testing can be a useful method of following
shone in the uninjured eye, and the perceived the course of traumatic conditions such as
brightness is assigned a value of 100% or $1.00. traumatic optic neuropathy. Amsler grid testing
When the light is shone in the involved eye, the can be used to detect and follow central
patient should provide the relative amount of scotomata.
brightness that is perceived (e.g. 50% or 50
cents).
Color vision testing and red desaturation testing Extraocular motility1,3,4
can help assess optic nerve function. Color vision Extraocular motility testing is especially impor-
can be tested using commercially available pseu- tant in cases of known or suspected orbital or
doisochromatic plates (e.g. Ishihara or Hardy- cranial nerve injury. Testing should be performed
Rand-Rittler). If color plates are not available, red after the possibility of an open globe injury has
desaturation testing can be used. The patient been excluded in order to minimize ocular
should look at a red object, typically the cap of a manipulation. Abnormal ductions and versions
dilating drop bottle, with each eye separately; if should be documented to allow comparison for
optic nerve dysfunction is present, the red color future examinations. In some circumstances
may appear gray or washed out compared to that (e.g. orbital fracture, traumatic 4th cranial nerve
seen by the uninvolved eye. palsy), diplopia or limitation of movement of the
It is important to note that subjective tests globe should be measured in prism diopters in
such as brightness and red desaturation testing, all directions of gaze, and the examiner should
variations in patient understanding and concom- attempt to isolate the affected extraocular
itant ocular injuries can make interpretation of muscle(s) or cranial nerves. This requires ade-
the examination unreliable. quate vision in both eyes as well as a conscious
and cooperative patient.
Visual fields1,4 If limitation of ocular motility is present,
In the emergency setting, testing visual fields forced duction testing may allow differentiation
by confrontation is effective and efficient. Each between a paretic and restrictive etiology. Forced
eye is tested separately. With one eye fully duction testing is performed as follows:
occluded, the patient should fi xate on the exam- 1. Topical anesthetic (e.g. proparacaine) is
iner’s face. The examiner’s fi ngers are presented administered.
in the four peripheral quadrants and centrally. If 2. A cotton-tipped applicator is soaked in 4%
fi ngers from both hands are presented simultane- lidocaine and placed for at least 1 minute on
ously in different quadrants, visual neglect may the conjunctiva over the extraocular muscle
be revealed. A red object may be used if visual to be tested.
23
Ocular trauma
3. The muscle insertion is grasped with toothed areas should be inspected for the presence of
forceps, and the eye is rotated in the direction ecchymoses, edema, ptosis, lacerations, and
opposite the muscle being tested. foreign bodies. The presence of enophthalmos or
Resistance to passive motion indicates a restric- exophthalmos should also be noted and may
tive etiology. Forced duction testing is typically require the use of a Hertel exophthalmometer.
reserved for patients with an orbital fracture and If ptosis is present, levator function and palpe-
suspected extraocular muscle entrapment. bral fi ssure size should be measured and
documented.
Intraocular pressure1,3 In the case of facial and eyelid lacerations,
It is prudent to defer measurement of intraocular dried blood may obscure the underlying tissues
pressure (IOP) until the presence or absence of and should be gently cleaned with gauze and
an open globe injury is determined. If a known sterile saline or hydrogen peroxide. The edges of
open globe injury is present, measurement of the laceration should be gently separated and the
IOP in the injured eye should be deferred until wound should be fully explored to assess its
after repair. depth and the presence of foreign bodies. Wounds
Various methods of measuring IOP are avail- that initially appear relatively superficial often
able, including Goldmann applanation tonome- are found to extend much deeper when they are
try, various hand-held tonometry devices properly cleaned and explored (Figure 3.3). In
(e.g. Tonopen), pneumotonometry, and Schiøtz cases of more severe periorbital injuries it may
tonometry. Applanation tonometry is the pre- be necessary to examine the patient under seda-
ferred method, but hand-held devices are tion or general anesthesia in order to assess ade-
extremely useful if the patient cannot be exam- quately the full extent of injury.
ined at the slit lamp. If no devices are available, Attention should be paid to lacerations that
globe palpation can provide an extremely gross involve the lid margin or the lacrimal drainage
estimate of comparative IOP. system. The use of toothed forceps to manipu-
Intraocular pressure can be low or high follow-
ing ocular trauma (Table 3.1). An abnormally
low IOP can indicate an occult open globe injury
but can also indicate ciliary body inflammation,
cyclodialysis, or a retinal detachment. A normal
or elevated IOP does not exclude the possibility of
an open globe injury. Acute elevation of IOP is
usually caused by aqueous humor outflow
obstruction in the setting of anterior chamber
inflammation, hyphema, angle closure (e.g.
pupillary block from a dislocated lens), and other
anatomic and inflammatory causes.
Figure 3.3 Eyelid lacerations must be fully explored to
External examination1,2 their fullest extent once globe integrity is confirmed
The head, face, periorbital areas, and eyelids and concomitant ocular injuries have been treated and
should be examined under good lighting. These stabilized.
24
Table 3.1 Causes of intraocular pressure (IOP) change following ocular trauma
Causes of high IOP Causes of low IOP Causes of high or low IOP
Lens-associated Excessive filtration Traumatic iridocyclitis
• Angle closure glaucoma • Wound leak (e.g. open globe • High IOP from inflammatory
secondary to pupillary block from injury) cells in anterior chamber
subluxated or dislocated lens • Ciliochoroidal detachment • Low IOP from ciliary body
• Phacomorphic glaucoma • Cyclodialysis cleft shutdown
• Lens particle glaucoma • Retinal detachment
• Phacoantigenic uveitis
Hemorrhage-associated Decreased aqueous production Cyclodialysis

• Hyphema • Intraocular inflammation • High IOP from closure of cleft
• Hemolytic glaucoma • Ciliary body ischemia/damage • Low IOP from increased
• Ghost cell glaucoma • Anterior proliferative aqueous outflow
vitreoretinopathy
Angle-associated
• Trabecular meshwork disruption
• Angle recession
• Peripheral anterior synechiae from
flat anterior chamber
Anterior chamber inflammation
Closure of cyclodialysis cleft
Epithelial downgrowth
Increased intraorbital pressure

• Retrobulbar hemorrhage
• Orbital emphysema from orbital
fracture
late canalicular lacerations should be avoided, as Conjunctiva1,3,4

further tissue damage can follow. The conjunctiva should be examined for the
The periorbital areas should be palpated for presence of chemosis, subconjunctival hemor-
crepitus (the perceived movement of subcutane- rhage, emphysema, foreign bodies (including
ous air) and orbital bony step-off deformities. contact lenses), abrasions, and lacerations. The
The function of the infraorbital nerve should presence of hemorrhagic chemosis may indi-
also be checked by gently stroking the upper cate an open globe injury, especially if it is
cheek below the eye with a cotton swab or present for 360 degrees or is accompanied by
similar item. Infraorbital hypesthesia, crepitus, subconjunctival pigmentation. Conjunctival em-
enophthalmos, and orbital deformity may physema (visible air in a subconjunctival
indicate the presence of an orbital blow-out location) may indicate the presence of a sinus
fracture. fracture. The detection of conjunctival abrasions
25
Ocular trauma
can be aided by the use of staining with fluores- A

cein or rose bengal. If a conjunctival laceration is
present, it is vital to rule out underlying scleral
lacerations or foreign bodies with a careful
examination under topical anesthesia.
Once it is determined that an open globe injury
is not present, the upper eyelid should be everted
and the superior tarsal conjunctiva should be
examined for the presence of foreign bodies. If
suspicion is present, the superior conjunctival
fornix can also be examined directly for the
presence of foreign bodies. This is accomplished
with ‘double eversion’ of the upper eyelid utiliz-
ing a Desmarres lid speculum inserted behind
the tarsal plate of the already everted upper B
eyelid (Figure 3.4A and B).
Cornea1,3,5
The cornea should be evaluated in a stepwise
fashion proceeding anteriorly to posteriorly. The
corneal epithelium should be examined for abra-
sions (with the use of topical fluorescein stain-
ing) and foreign bodies. The presence of either
should prompt an examination of the tarsal con-
junctiva to rule out a foreign body. Linear corneal
abrasions should increase suspicion for one or
more subtarsal foreign bodies.
The corneal stroma should be evaluated for the
presence, location, length, width, and depth of Figure 3.4 After eversion of the upper eyelid (A), a
Desmarres retractor is inserted behind the tarsal plate
foreign bodies, lacerations, and ulcerations; such
and gentle traction away from the globe is introduced
fi ndings should be drawn in the medical record. (B), exposing the superior conjunctival fornix.
If a laceration is present, a Seidel test (Figure
3.5) is used to determine if it is full thickness:
1. A dense layer of fluorescein dye is applied to
the suspicious area, which is then examined 3. It may be necessary to apply gentle pressure
under cobalt blue light. on the upper or lower bulbar conjunctiva
2. If aqueous fluid is leaking through the wound, to fully elicit a wound leak in questionable
it will be seen as a bright green stream within cases. This should be performed with great
the darker pool of dye. Fluorescein dye in high care.
concentration does not fluoresce and appears In cases of microbial keratitis (corneal ulcer), the
dark, and leaking aqueous dilutes the dye to cornea should be scraped for microbiologic iden-
a concentration that creates fluorescence. tification via smears and cultures.
26
A B
Figure 3.5 A 52-year-old male presents with pain and

discomfort in his right eye. A history of distant trauma
was elicited, though the exact mechanism was unclear. A
Seidel test was performed over the area marked with the
black arrow (A). Aqueous is seen exiting through the
fluorescein that has been painted over the suspicious
area (B) in a characteristic fashion that denotes a positive
Seidel test (C).
Descemet’s membrane and the corneal endo- Anterior chamber1,2

thelium should be examined for discontinuities, The depth of the anterior chamber should be
breaks, and folds, especially in the presence of assessed. An abnormally deep chamber can be
overlying stromal edema. Birth trauma, typically caused by a posterior scleral rupture, posteriorly
during a forceps delivery, can cause vertical dislocated lens, cyclodialysis, or iridodialysis. A
breaks in Descemet’s membrane with associated shallow anterior chamber can signify a full-
corneal stromal edema and corneal clouding. thickness corneoscleral wound, anteriorly dislo-
In the case of chemical burns, the extent of cated lens, suprachoroidal hemorrhage, serous
corneal epithelial erosion and stromal haze choroidal detachment, or intumescence of the
should be documented. The surrounding limbus, lens after rupture of the lens capsule (Figure 3.6).
conjunctiva, and sclera should be examined for In the absence of an open globe injury, gonios-
ischemic necrosis and blanching of vessels. The copy is used to examine the anterior chamber
presence of limbal blanching portends a guarded angle. It is preferable to use a four-mirror lens
prognosis because the limbus contains the stem that does not require a gel-coupling medium to
cells of the corneal epithelium. minimize pressure or traction on the globe.
27
Ocular trauma
iris should also be inspected. An abnormal

contour raises suspicion for localized iris injury
or injury to structures posterior to the iris,
such as lens capsule rupture or ciliary body
detachment. Direct illumination and retroillu-
mination of the iris can reveal iridodialysis, iris
sphincter tears, and holes or perforations from
intraocular foreign bodies. Diffuse damage to
the iris sphincter causes traumatic mydriasis.
Traumatic instability of the iris–lens diaphragm
causes iridodonesis, a shimmering or floppiness
seen during eye movement.
Figure 3.6 A thin slit beam best demonstrates the
depth of the anterior chamber. A contusive injury to The shape of the pupil should be noted. An
the eye caused a rupture of the anterior lens capsule eccentric or peaked pupil may indicate a trau-
and the rapidly progressive cataract seen in this photo. matic iridodialysis, iris sphincter tear, vitreous
The anterior chamber depth was severely shallow in prolapse into the anterior chamber, or an open
comparison to the fellow uninjured eye. globe injury with iris prolapse.
Lens1,3
Gonioscopy allows examination for iridodialysis, The crystalline lens should be examined for its
cyclodialysis, angle recession, and foreign bodies position, stability, clarity, and capsular integrity.
in the angle. This is particularly important if a The presence of lens subluxation or dislocation
small full-thickness corneal wound is present should be noted. Phacodonesis, or shaking of the
without further injury to the iris or lens, as lens with eye movements, should be specifically
foreign bodies in the inferior angle can easily be tested. The presence of vitreous around the lens
missed without gonioscopy. indicates zonular rupture and lens instability. In
The anterior chamber should also be examined cases of severe trauma, the lens can be extruded
for the presence of cells and flare, indicating a completely from the eye through a scleral or
traumatic iritis. The inflammatory reaction corneal wound. In pseudophakic patients,
should be graded to allow comparison with extrusion of an intraocular lens can occur
future examinations. The presence of hyphema through dehiscence of a prior surgical wound,
and hypopyon should be noted, and the height particularly ruptured penetrating keratoplasty
of each in millimeters should be documented. or extracapsular cataract surgery wounds.
The presence of fibrin, vitreous, or foreign The clarity of the lens can be evaluated
bodies in the anterior chamber should also be with direct illumination and retroillumination.
noted. Numerous lens changes can occur after trauma,
including rosette-shaped posterior subcapsular
Iris1 cataracts, anterior subcapsular opacities, and
The iris should be inspected prior to the instil- sectoral cataracts. A contusive injury can create
lation of mydriatics, as dilation may obscure per- a Vossius ring, a brown ring of pigment on the
tinent fi ndings. The surface of the iris should be anterior lens capsule resulting from forceful
examined for foreign bodies. The contour of the iridolenticular contact (Figure 3.7).
28
posterior segment can be assessed with an

examination through a nondilated pupil and
with ancillary studies such as ultrasonography
and computed tomography.
Scleral depression is essential in evaluating
possible peripheral vitreoretinal pathology, but
it should be deferred in cases of open globe
injury, acute hyphema, recent ocular surgery,
and significant periocular injury (e.g. orbital
fracture, large lid laceration).
All posterior segment fi ndings should be docu-
mented with a detailed drawing in the medical
Figure 3.7 A Vossius ring is seen on the anterior lens
record.
capsule following an assault-related contusive injury in
a 42-year-old male. Significant subconjunctival
hemorrhage and a small hyphema are also noted. Vitreous1,4
The anterior, mid, and posterior vitreous should
be examined for the presence of pigment
It is important to note the integrity of the lens (‘tobacco dust’), hemorrhage, debris, and foreign
capsule, as a violation of the capsule may indi- bodies. The presence of a Weiss ring, indicating
cate the presence of a foreign body. It is also a posterior vitreous detachment (PVD), should
important to note any leakage of cortical mate- be noted. Tobacco dust and/or vitreous hemor-
rial due to its antigenic nature. Intralenticular rhage should prompt a search for a traumatic
foreign bodies should be noted as well. PVD or retinal tear. Vitreous streaming toward
the anterior segment or pars plana may reveal an
General principles of the posterior occult open globe injury. The presence of white
segment examination1,2,4 blood cells or purulence in the vitreous cavity
The posterior segment should be examined as should prompt collection of vitreous samples for
expeditiously as possible since progressively microbiologic identification.
difficult visualization can occur from corneal Vitreous in the anterior chamber has a unique
edema, hyphema, traumatic cataract, vitreous appearance of a gelatinous material with small,
hemorrhage, etc. The type, strength, and time of brown pigmented spots intermixed and indicates
mydriatic use should be documented in the significant damage to the zonular apparatus.
medical record so that subsequent examiners Because of the higher molecular weight of vitre-
will not misinterpret the cause of dilated pupils ous compared to aqueous, the pupil is normally
(on multiple occasions, we have seen CT scans distorted in the vicinity of vitreous prolapse.
ordered on post-trauma patients because of Phacodonesis, lens subluxation, or frank lens dis-
undocumented dilation of the pupils). When an location often coexists with vitreous prolapse.
open globe injury is suspected, any topical medi-
cations should be given from unopened sterile Retina and choroid1,4
bottles to avoid possible infection. Pharmaco- The retina should be carefully and thoroughly
logic mydriasis should be deferred in the case of examined for the presence of whitening and
an open globe injury with iris prolapse; the edema (commotio retinae), tears, holes (periph-
29
Ocular trauma
eral and macular), dialysis, and detachment.

Scleral depression is necessary to examine the
far periphery, but is often deferred during the
acute post-traumatic period.
The location of hemorrhage relative to the
retina can indicate the site of injury. Vitreous
hemorrhage can indicate the presence of a trau-
matic PVD or retinal tear. Hemorrhage within
the retinal nerve fiber layer appears linear or
flame-shaped, while hemorrhage within the
deeper retinal layers appears as irregular blotches.
Subretinal hemorrhage appears dark and homo-
Figure 3.8 Peripapillary intraretinal hemorrhage with
geneous and is a clue to the presence of choroidal
breakthrough vitreous hemorrhage following optic
rupture. The area surrounding intraretinal or
nerve avulsion in a 10-year-old child.
subretinal hemorrhages should be carefully
examined for the presence of foreign bodies or
occult open globe injuries. SPECIAL CONSIDERATIONS FOR
The choroid should be examined for the pres- PEDIATRIC PATIENTS5
ence of choroidal rupture and choroidal detach-
ment. Choroidal ruptures are often multiple, The history in cases of pediatric ocular trauma
concentric to the optic disc, and accompanied by is frequently elicited from the child’s caregiver
subretinal hemorrhage. (usually the child’s parents). However, in cases
of poor supervision or child abuse, the history
Optic nerve1 from the caregiver may not be accurate. Older
The optic nerve head should be inspected for children sometimes fear disciplinary action and
the presence of edema and hemorrhage. The size may not provide the entire truth if they were
and shape of the cup should be documented. An engaged in prohibited activities.
enlarged cup or other signs of previous glauco- Examining the eyes of a child is challenging
matous damage may require more aggressive under ideal circumstances and can verge on
intraocular pressure control as compared to a impossible when a child is injured. Establishing
normal nerve. a rapport and interacting with the child in a
In cases of severe trauma, the optic nerve can game-like fashion may help maintain the child’s
be partially or completely avulsed. This is seen attention. The noncontact portions of the exam
as an absence of the optic disc or a hole in the should be performed fi rst, and no pressure should
sclera at the site of the disc (Figure 3.8). Despite be placed on the globe. Explaining each part of
significant contusive injury, the optic nerve often the exam as it is performed may reduce anxiety
appears normal immediately following trauma on the part of the caregiver.
and is therefore of limited value in cases of sus- For children between the ages of 10 weeks and
pected traumatic optic neuropathy. 3 years, the visual acuity in each eye should be
tested as the ability to fi xate on an object with
smooth pursuit (fi x and follow). The object can
30
be a colorful toy or an adult’s face, but should 3. The child’s head is placed on the assistant’s
not be a light source. It should be confi rmed that lap.
the child is following the visual stimulus and not 4. The caregiver holds the child’s hands and the
any auditory stimuli that may arise from it. For assistant holds the child’s head still while the
older children, visual acuity can be assessed with physician examines the child.
Allen cards, HOTV letters, the tumbling E Sometimes it is more feasible for the physician
game, or standard visual acuity charts depend- to take the place of the assistant and control the
ing on the child’s age and education level head with his legs while performing the exami-
(Table 3.2). nation (Figure 3.9).
If an infant or toddler is very uncooperative, If the above methods are not sufficient or if an
the child can be restrained in a commercially open globe injury is suspected, the child should
available or makeshift papoose. A pediatric be examined under conscious sedation or general
eyelid speculum with the use of topical anesthe- anesthesia. This should be carried out under
sia can be used, but only if an open globe injury the supervision of a qualified anesthesiologist.
is not suspected. Toddlers can also be restrained Vital signs should be monitored during the
as follows: examination, and advanced cardiopulmonary
1. An assistant and caregiver sit facing each other life support measures must be present and
at the same level. available. Pediatric clearance should be obtained
2. The child is placed supine with legs straddling prior to any examination requiring general
the caregiver’s waist. anesthesia.
Table 3.2 Normal visual acuity in children as measured by various tests
Age (years) Vision test Normal acuity
0–2 Visual evoked potential 20/60–20/20 (6 months)

20/40–20/20 (1 year)
0–2 Forced choice preferential looking 20/200 (6 months)

20/50 (1 year)
20/30 (2 years)
0–2 Fixation behavior Central, steady, maintained
0–3 Opticokinetic nystagmus test 20/200 (6 months)

20/80 (1 year)
20/20 (2–3 years)
2–5 Allen pictures 20/40–20/20
2–5 HOTV test 20/40–20/20
2–5 ‘E’ game 20/40–20/20
5+ Snellen chart 20/30–20/20
31
Ocular trauma
Figure 3.10 Bilateral fundus photographs of an infant

show bilateral intraretinal and preretinal hemorrhage
due to shaken baby syndrome. The round peripheral
intraretinal hemorrhages, some with white centers,
are typical but not specific to the diagnosis of shaken
baby syndrome. Careful, sequential photographic
documentation is of utmost importance as criminal
Figure 3.9 Examination technique for pediatric
proceedings are commonplace. The assailant in this
patients. The parent or guardian controls the legs
case was a family member acting as a babysitter for the
and arms while the physician controls the head.
infant.
Alternatively, an assistant can be seated opposite the
parent and control the head leaving the physician with
more flexibility to examine the patient.
should be suspected when the caregiver’s history
is inconsistent, the child has a history of multiple
Examination of the anterior segment can be emergency room visits, or the character of the
facilitated by a penlight or portable slit lamp. If injury is not compatible with the caregiver’s
the child is old enough to undergo a conventional history. The ocular examination can play an
slit lamp examination, he or she can sit on the important role in the diagnosis of shaken baby
caregiver’s lap, kneel on the exam chair, or stand syndrome. In this syndrome, intraocular and
on the exam chair’s step. Alternatively, an indi- intracranial hemorrhages are present, often
rect ophthalmoscopy lens with a light source without external signs of trauma. Ocular hemor-
(e.g. indirect ophthalmoscope) may provide rhages are usually intraretinal but can be prereti-
enough magnification to examine the anterior nal or subretinal as well (Figure 3.10).5
segment. All light sources should be used at low Physicians are legally mandated to report
intensity if possible. cases of suspected child abuse to the appropriate
Eye drops are often a source of anxiety for social service agency or the police. A reason-
children. For mydriasis, a combination of able suspicion of child abuse exists when it is
phenylephrine 2.5%, tropicamide 0.5%, and part of the differential diagnosis. Most states
cyclopentolate 0.5% can be prepared so that have laws protecting a reporting practitioner
all three medications can be instilled with with good intentions from civil liability. Failure
one drop. Instilling topical anesthesia prior to to report is a misdemeanor in most states.
mydriatics can reduce discomfort and increase Accurate and detailed documentation of the
cooperation. history and examination in the medical record
(including photography if available) is of
Child abuse utmost importance, as this information often
The ophthalmologist should be alert for ocular is submitted as evidence in a deposition or trial.
and systemic signs of child abuse. Child abuse The examining physician should also expect
32
to serve as a material witness for any legal giver. The patient may appear withdrawn,
proceedings.6 depressed, or anxious, and the caregiver may
give an inconsistent history. As with child abuse,
the physician should intervene with the aid of
SPECIAL CONSIDERATIONS FOR the appropriate social services.7
ELDERLY PATIENTS4
As with pediatric patients, some elderly patients RADIOLOGIC IMAGING

may not be able to provide an adequate history
because of underlying disability or dementia. Several types of imaging studies are of great
The history is often elicited from family members utility following ocular and periocular trauma.
or caregivers, but the history may not be accurate In general, these techniques should be employed
if elder abuse is involved. if the posterior pole is not adequately visualized
Falls are a common cause of injury in elderly or if orbital fractures, optic canal impingement,
patients, and it is important to investigate the intraocular foreign bodies, or intraorbital foreign
circumstances surrounding the fall. Many falls in bodies are suspected.
this age group are a result of disorders of gait or
balance. However, falls due to syncope or loss of
consciousness may point toward underlying car- Plain radiography
diovascular dysfunction (e.g. arrhythmia, hypo- With the advent of modalities such as computed
tension) that warrants further attention. tomography (CT) and magnetic resonance
Ocular and periocular injuries from falls in the imaging (MRI), the use of plain radiography has
elderly are frequently associated with systemic diminished significantly. However, it may be
injuries, often serious. These include fractures employed when these other techniques are not
(hip, long bones, skull, wrist) and internal readily available.
hemorrhage (intracranial, intra-abdominal). The
latter may be facilitated by anticoagulation Indications:
therapy. If the ophthalmologist is the fi rst physi- 1. To determine the presence and location of
cian to encounter such a patient, a rapid assess- intraocular and intraorbital foreign bodies and
ment for these injuries should be performed orbital fractures only when CT and MRI are
before focusing attention on the eye. Conditions not available.
such as respiratory distress, cardiovascular 2. To screen for the presence of metallic foreign
instability, massive bleeding, or acutely impaired bodies prior to MRI imaging.8
mental status require immediate transfer to an
emergency room or trauma center. Advantages:
As with child abuse, a high level of suspicion 1. Readily available at most medical facilities.
should be maintained about the possibility of 2. Bony structures are visualized.
elder abuse or neglect. Elder abuse includes any
pattern of behavior that causes physical, psycho- Disadvantages:
logical, sexual, fi nancial, or social harm to an 1. Does not detect radiolucent foreign bodies
older person. The perpetrator often is a family (e.g. plastic, wood). 9
member (most commonly the spouse) or care- 2. Does not visualize soft tissues well.
33
Ocular trauma
Computed tomography2,10
Computed tomography (CT) has replaced plain
radiography as the preferred imaging modality
for ocular and periocular trauma. Both axial
(1.0–2.0 mm sections) and coronal (2.0–4.0 mm
sections) views should be obtained to best local-
ize foreign bodies or fractures in three dimen-
sions. Axial sections provide the best views of
the globe, the medial and lateral rectus muscles,
and the medial and lateral walls of the orbit.
Coronal sections provide the best views of the
superior and inferior rectus muscles and the
orbital roof and floor. Intravenous contrast is
rarely necessary in the setting of acute ocular or
periocular trauma.
Indications:
1. Suspected open globe: Findings suggestive of Figure 3.11 A glass intraocular foreign body is readily
a ruptured globe include eyewall deformity seen on this coronal computed tomography scan.
or wound, intraocular air, intraocular foreign
body, and intraocular hemorrhage. 5. Visualizes fresh blood (without contrast
2. To visualize the posterior segment when it is enhancement).
not visualized on clinical examination and 6. Can be performed on patients with suspected
ultrasonography is not available. or known metallic foreign bodies, those with
3. To determine the presence and location of pacemakers, and those on life support.
suspected intraocular or intraorbital foreign 7. Compared to MRI, CT is faster, less expen-
bodies (Figure 3.11). sive, produces less motion artifact, and is less
4. To determine the presence and location of likely to induce claustrophobia.
orbital fractures.
5. To determine the presence and location of Disadvantages:
intracranial or intraorbital hemorrhage. 1. May not be readily available if the patient
presents in an office-based setting.
Advantages: 2. Generally contraindicated in pregnant women
1. Readily available at most medical facilities. due to radiation exposure.
2. No direct contact with the eyelids or globe is 3. Resolution of intraocular structures is not as
necessary. high as ultrasonography.
3. Visualizes both soft tissues and bony 4. Proper positioning for direct coronal scans
structures. may not be possible for traumatized or unco-
4. Visualizes both radio-opaque (e.g. iron, glass, operative patients. In these cases, coronal
graphite) and radiolucent foreign bodies with reconstructions from axial images may be uti-
excellent resolution capabilities. lized, but these images are of somewhat lower
34
quality than direct coronal images. Alterna- and the most detailed anatomic information
tively, helical or spiral CT scanning can regarding the posterior segment of the eye. It
provide better coronal images if this tech- has a resolution ranging from 0.1 to 0.01 mm.
nique is available.11 Standard B-scan ultrasonography can visualize
radio-opaque and radiolucent intraocular foreign
Magnetic resonance imaging2,10 bodies as well as pathology of the following
The role of magnetic resonance imaging (MRI) structures:
in the setting of acute ocular and periocular 1. Vitreous (opacities, hemorrhage, posterior
trauma is not well defi ned. MRI best visualizes vitreous detachment)
vascular lesions, intracranial processes, cavern- 2. Retina (tears, detachment)
ous sinus thrombosis, and inflammatory and 3. Choroid (serous choroidal detachment, supra-
demyelinating optic nerve conditions. choroidal hemorrhage, rupture)
4. Sclera (rupture).
Indications: It can also be used to visualize orbital structures
1. To visualize periocular soft tissues. such as the lacrimal gland, extraocular muscles,
2. To visualize suspected vascular lesions, intra- optic nerve, and orbital soft tissues. Ultrasound
cranial pathology, and optic nerve lesions. biomicroscopy utilizes higher sound wave fre-
3. To locate non-magnetic intraocular or intra- quencies to provide detailed images of the ante-
orbital foreign bodies. rior segment and its pathology, including occult
foreign bodies.12
Advantages:
1. Produces axial, coronal, and sagittal views Indications:
without repositioning the patient. 1. To evaluate the posterior segment when an
2. Soft tissue imaging is superior to that of CT. adequate view is not possible on clinical
3. Visualizes non-magnetic foreign bodies. examination.
4. Can be used in pregnant women. 2. To determine the presence and location of
intraocular (Figure 3.12) and intraorbital
Disadvantages: foreign bodies.
1. Not as widely available as CT.
2. Relatively long acquisition time, which can Advantages:
produce motion artifact and claustrophobia. 1. Provides the highest resolution of intraocular
3. Contraindicated in patients with suspected structures compared to CT and MRI.
magnetic intraocular or intraorbital foreign 2. Provides real-time cross-sectional and radial
bodies, pacemakers, cochlear implants, and views of the globe.
life support equipment. 3. The equipment is relatively mobile, allowing
4. Does not visualize bony structures as well as rapid imaging in a clinic setting, at the bedside,
CT. or in the operating room.
Ultrasonography2,10 Disadvantages:
Of all of the imaging modalities discussed, ultra- 1. Requires a trained and experienced techni-
sonography (US) provides the greatest resolution cian to provide optimal results, although non-
35
Ocular trauma
trained personnel can use it as a screening tool

in an emergency setting.13
2. Requires direct contact with the eyelids or
globe and requires extreme caution if used in
the setting of an open globe injury.
3. Cannot be used to visualize orbital
fractures.
Figure 3.12 A highly reflective foreign body on the

surface of the retina is seen on B-scan ultrasonography.
Note the orbital shadowing induced by the foreign
body.
Appendix: Examination pearls
Examination pearls for suspected subtarsal foreign body
Slit lamp exam
• Vertical, linear corneal abrasions

• Conjunctival abrasions
Techniques
• Upper eyelid eversion (to examine superior tarsal conjunctiva)

• Double eyelid eversion using Desmarres lid retractors (to examine superior conjunctival
fornix)
Examination pearls for chemical injury
Techniques
• Copious irrigation, prior to taking a history or performing an examination

• Determining approximate pH of chemical and pH of involved eye
Slit lamp exam
• Corneal epithelial erosion

• Corneal stromal haziness
• Blanching of limbal vessels
36
Appendix: Examination pearls—cont’d
Examination pearls for suspected orbital floor fractures
External exam
• Crepitus (the presence of mobile air in the subcutaneous tissues)

• Orbital bony step-off deformities
• Infraorbital hypesthesia
Motility
• Restriction of upgaze (using forced ductions if necessary)

Exam techniques
• Exophthalmometry (usually enophthalmic, but may be exophthalmic initially due to swelling

and edema)
Imaging
• CT scan of orbits (axial and coronal views)
Examination pearls for suspected open globe injury
Slit lamp exam
• Eccentric or peaked pupil

• Low intraocular pressure (relative to fellow eye)
• Hemorrhagic chemosis (especially 360 degrees)
• Conjunctival and scleral lacerations
• Shallow or abnormally deep anterior chamber
• Vitreous streaming toward pars plana or anterior chamber
• Subconjunctival pigment
Imaging
• CT scan of orbit or ocular ultrasound (look for eyewall deformity or wound, intraocular air,
intraocular foreign body, intraocular hemorrhage)
37
Ocular trauma
Appendix: Examination pearls—cont’d
Examination pearls for suspected intraocular foreign body
Slit lamp exam
• Conjunctival, corneal, and scleral lacerations

• Iris transillumination defects
• Lens capsule rupture and/or focal lens opacity
• Intralenticular foreign body
• Posterior segment foreign body
Techniques
• Gonioscopy (four-mirror lens that does not require gel-coupling medium) to rule out anterior
chamber angle foreign body
Imaging
• CT scan of orbits with fine axial and coronal cuts
8. Seidenwurm DJ, McDonnell CH 3rd, Raghavan N, Breslau J.

REFERENCES Cost utility analysis of radiographic screening for an orbital
foreign body before MR imaging. Am J Neuroradiol
1. Hamill MB. Clinical evaluation. In: Shingleton BJ, Hersh PS, 2000;21:426–433.
Kenyon KR, eds. Eye Trauma. St. Louis: Mosby Year Book; 9. Lagalla R, Manfre L, Caronia A, Bencivinni R, Duranti C,
1991:3–24. Ponte F. Plain film, CT and MRI sensibility in the evaluation of
2. Harlan JB Jr, Ng EWM, Pieramici DJ. Evaluation. In: Kuhn F, intraorbital foreign bodies in an in vitro model of the orbit
Pieramici DJ, eds. Ocular Trauma: Principles and Practice. and in pig eyes. Eur Radiol 2000;10:1338–1341.
New York: Thieme; 2002:52–69. 10. Joseph DP, DiBernardo C, Miller NR. Radiographic and
3. Freeman HM, McDonald PR, Scheie HG. Examination of the echographic imaging studies. In: MacCumber MW, ed.
traumatized eye and adnexa. In: Freeman HM, ed. Ocular Management of Ocular Injuries and Emergencies.
Trauma. New York: Appleton-Century-Crofts; 1979:1–13. Philadelphia: Lippincott-Raven; 1998:55–77.
4. Congdon NG, MacCumber MW. Ocular evaluation. In: 11. Lakits A, Prokesch R, Scholda C, Bankier A. Orbital helical
MacCumber MW, ed. Management of Ocular Injuries and computed tomography in the diagnosis and management of
Emergencies. Philadelphia: Lippincott-Raven; 1998:29–54. eye trauma. Ophthalmology 1999;106:2330–2335.
5. Fard AK, Repka MX. Special issues in pediatric ocular trauma. 12. Deramo VA, Shah GK, Baumal CR et al. Ultrasound
In: MacCumber MW, ed. Management of Ocular Injuries and biomicroscopy as a tool for detecting and localizing occult
Emergencies. Philadelphia: Lippincott-Raven; 1998:39–54. foreign bodies after ocular trauma. Ophthalmology
6. Halverson KC, Elliott BA, Rubin MS, Chadwick DL. Legal 1999;106:301–305.
considerations in cases of child abuse. Primary Care 13. Blaivas M, Theodoro D, Sierzenski PR. A study of bedside
1993;20:407–415. ocular ultrasonography in the emergency department.
7. Lachs MS, Pillemer K. Elder abuse. Lancet 2004;364:1263–1272. Acad Emerg Med 2002;9:791–799.
38
4
Definitions and classification
in ocular trauma
James T. Banta
INTRODUCTION ambiguity, especially between healthcare

professionals.
Inherent difficulties will always exist in the eval- The protean manifestations of ocular trauma
uation of eye trauma. A seemingly white and have long hobbled attempts at creating a mean-
quiet eye can be rendered sightless from optic ingful, clinically sound, and reproducible classifi-
nerve injury (i.e. traumatic optic neuropathy or cation system. Clearly, the ability to communicate
optic nerve avulsion) whereas an eye swollen in a logical, formatted fashion is desirable, other-
shut and diffusely hemorrhagic can appear dra- wise collecting data and drawing comparisons
matically damaged, yet quickly recover normal between similar groups becomes increasingly dif-
vision. This is a primary reason for systemati- ficult. Likewise, communications between health
cally approaching the evaluation of eye trauma professionals is greatly hampered without a uni-
patients. Furthermore, defi ning a uniform termi- versally accepted vocabulary. Only in the last
nology and classification scheme for ocular decade, through the determined work of a few
trauma is necessary to prevent confusion and eye trauma pioneers, has this goal been attained.
DEFINITIONS
Example 1
‘Doc, we’ve got a ruptured globe we’d like to send you. The young man has a double-penetrating,
through and through injury. The perforation is visible at the edge of the cornea.’
Working in an eye emergency room, I have often heard similar descriptions of eye injuries
from both ophthalmologists and non-ophthalmologists. Could you assess the extent of injury
from this statement? Could you determine the mechanism of injury? Is an intraocular foreign
body a possibility? Do any ancillary studies need to be performed before the patient is trans-
ferred? This example illustrates the need for a uniform classification scheme so that appropriate
triage of patients and effective communication between healthcare professionals can be
accomplished.
Ambiguous terminology hampers effective com- dite appropriate diagnostic procedures and
munication, particularly between healthcare referrals and, conversely, to avoid unnecessary
professionals. Never has this been more apparent tests and consultations. Ruptured globe, open
than with eye traumatology terms. Terms need globe, and globe laceration are often incorrectly
to be specific and unambiguous, both to expe- used interchangeably. Penetrating and perforating
39
Ocular trauma
Figure 4.1 Physiology of an eyewall rupture. When a Blunt object approaching

blunt object strikes the eye with significant force, the eye at high speed
intraocular pressure suddenly and violently increases. If
the intraocular pressure becomes greater than the
weakest breaking point of the eyewall (typically
adjacent to the insertions of the rectus muscles or sites
of previous surgery), intraocular contents are forced
through the break in the eyewall with tremendous
force, leading to extensive intraocular disruption.
▲
Object strikes eye at
injuries are still frequently confused or used
high velocity causing
interchangeably. A review of past ophthalmic a sudden rise in
literature reveals many redundancies and ambi- intraocular pressure
guities, further clouding the situation. A con- depicted by arrow
certed effort in the mid-1990s led to a widely
accepted, standardized classification of ocular
trauma.1,2
Table 4.1 lists the defi nitions of the standard-
ized ocular traumatology terms. 3 Defi nitions
stem from regarding the entire globe as the tissue
of reference, rather than clouding the issue with
When the intraocular
tissue-specific descriptions. These terms should pressure is high
be committed to memory and used appropri- enough, a break
ately while abandoning ambiguous and often in the eyewall
occurs leading
incorrect terminology. Not everything is a rup-
to extrusion of
tured globe! intraocular contents
An important distinction that merits special
attention is the use of ‘rupture’ and ‘laceration’
when describing an open globe injury. Rupture
implies a severe blow from a blunt object to the
eyewall, leading to deformation of the globe. The
fluid within the eye is incompressible, creating a
After the injury,
rapid, violent rise in intraocular pressure. If the severe intraocular
pressure is high enough or the eyewall is weak disruption is present
enough, an inside-out force creates a break in the
eyewall’s weakest point. Intraocular contents are
often extruded due to the direction and force of
the energy created, frequently with devastating
effects (Figure 4.1). Conversely, a laceration is a
violation of the eyewall created by a sharp object
in an outside-in fashion. Although highly variable
40
Definitions and classification in ocular trauma
Table 4.1 Ocular traumatology definitions (Birmingham Eye Trauma Terminology).
Terms and definitions in BETT a

Term Definition/interpretation Explanation
Eyewall Sclera and cornea Though technically the eyewall has three
coats posterior to the limbus, for clinical
and practical purposes, violation of only
the most external structure is taken into
consideration
Closed globe injury No full-thickness wound of eyewall
Open globe injury Full-thickness wound of the eyewall
Contusion No (full-thickness) wound The injury results from direct energy
delivery by the object (e.g. choroidal
rupture) or from the changes in the
shape of the globe (e.g. angle recession)
Lamellar laceration Partial-thickness wound of the The wound of the eyewall is not
eyewall ‘through’ but ‘into’
Rupture Full-thickness wound of the eyewall Because the eye is filled with
caused by a blunt object incompressible liquid, the impact results
in momentary increase of the intraocular
pressure. The eyewall yields at its
weakest point (at the impact site or
elsewhere; e.g. an old cataract wound
dehisces even though the impact
occurred elsewhere). The actual wound is
produced by an inside-out mechanism
Laceration Full-thickness wound of the eyewall The wound occurs at the impact site by
caused by a sharp object by an outside-in mechanism
Penetrating injury Entrance wound If more than one wound is present, each
must have been caused by a different
agent
Intraocular foreign body Retained foreign object(s) Technically this is a penetrating injury
but grouped separately because of
different clinical implications
Perforating injury Entrance and exit wounds Both wounds are caused by the same
agent
a
Some injuries remain difficult to classify (an intravitreal BB pellet) whereas technically an intraocular foreign
body (IOFB) injury is a blunt object that requires great force to enter the eye, involving an element of rupture.
In such situations, the ophthalmologist should describe the injury as ‘mixed’ (i.e., rupture with an IOFB) or
select the most serious type of the mechanisms involved.
(From Kuhn F, Morris R, Witherspoon CD. Birmingham Eye Trauma Terminology (BETT): terminology and
classification of mechanical eye injuries. Ophthalmol Clin N Am 2002;15:139–143, with permission of Elsevier.)
41
Ocular trauma
Figure 4.2 Physiology of an eyewall laceration. When a

sharp object strikes the eye, little force is needed to
penetrate the eyewall; therefore the intraocular
pressure is increased only mildly. When the sharp
object is removed, only local disruption at the entry/
exit site is seen.
▲
depending on the mechanism of injury, the vector
forces created are typically less than those seen
with blunt objects, resulting in less of an intra-
ocular pressure elevation, and oftentimes less
extrusion of intraocular contents (Figure 4.2).
A second frequent area of confusion is with the Sharp object approaches the eye at a high velocity
terms ‘penetration’ and ‘perforation.’ Penetra-
tion and perforation imply a violation of the
eyewall (open globe injury), typically by a sharp
object, but differ in the location of the entry and
exit wounds. Figure 4.3 illustrates the differ-
ence. The entry and exit wounds in a penetrating
injury are the same (Figure 4.3A), implying a
sharp object has entered the eye and then come
back out of the same wound (e.g. stab wound).
Separate entry and exit wounds are found in a
perforating injury (Figure 4.3B), implying the
same sharp object has entered the eye at one
location and had enough momentum to exit the
eye from a separate location. If the inciting object Sharp object pierces the eye, causing only a mild rise
causing the eyewall wound enters and remains in intraocular pressure
within the eye, a penetrating injury with an
intraocular foreign body is seen (Figure 4.3C).
The blame for the confusion can be laid directly
on the lack of standardized terminology over
the years. Until the mid-1990s, publications in
peer-reviewed journals of ophthalmology con-
cerning ocular trauma often used redundant
and sometimes confl icting terms, further propa-
gating the confusion. As an example, the follow-
ing is a direct quote from a paper published in
a respected ophthalmic publication: ‘In 6 cases
(2%) there was a double perforation, and the
IOFB was found behind the globe.’ What is a Sharp object is removed from the eye and only minimal
‘double perforation’? How can an intra-ocular intraocular disruption is seen at the wound
42
A Entry wound Exit wound
Sharp
object
B Object approaching eye Entry wound

with velocity
Object leaving eye

with velocity Exit wound
C Object approaching eye Entry wound

with velocity
Object within eye at less velocity
Intraocular foreign body
Figure 4.3 Schematic illustration of the differences between an eyewall penetration (A), eyewall perforation (B),
and an intraocular foreign body (C).
foreign body (IOFB) be found behind the globe? simple yet comprehensive classification scheme
Needless to say, this ambiguous terminology is that removes ambiguity and redundancy. It has
unacceptable. been endorsed by the American Academy of
Ophthalmology, the International Society of
STANDARD TERMINOLOGY Ocular Trauma, the World Eye Injury Registry,
and the Vitreous and Retina Societies. Its
Once a unified set of defi nitions is available, a use is mandatory for publication in a multitude
coherent terminology system is possible. Created of scientific journals (e.g. Ophthalmology,
simultaneously with the accepted defi nitions Graefe’s Archive for Clinical and Experimental
described previously, the ocular traumatology Ophthalmology).
system,1–3 more recently revised as the Birming- Figure 4.4 shows the pathway to making a
ham Eye Trauma Terminology (BETT),4 is a correct diagnosis. The fi rst question faced is
43
Ocular trauma
Eye injury
Is a full-thickness
eyewall defect present?
No Yes
Closed globe Open globe
Is a partial-thickness Was the injuring object

eyewall defect present? blunt or sharp?
No Yes Blunt Sharp
Contusion Lamellar Rupture Laceration

laceration
Same entry and Retained Different entry

exit wound foreign body and exit wounds
Penetration IOFB Perforation

Figure 4.4 Flow diagram for making appropriate ocular trauma diagnosis. (After Kuhn F, Morris R, Witherspoon
CD. Birmingham Eye Trauma Terminology (BETT): terminology and classification of mechanical eye injuries.
Ophthalmol Clin N Am 2002;15:139–143, with permission of Elsevier.)
44
always, ‘Is there a full-thickness defect of the By using the eyewall as the frame of reference,
eyewall?’ If not, the closed globe injury is sepa- confusion is limited. For example, a penetrating
rated into contusions (typically caused by a blunt scleral wound refers to an entry into but not
object) and lamellar lacerations (typically caused through the sclera. This would be a closed globe
by a sharp object). If a full-thickness defect injury (lamellar laceration by BETT), but could
(open globe injury) is discovered, the next ques- easily be mistaken for an open globe injury. Con-
tion is ‘Was the injuring object, sharp or blunt?’ versely, a perforating scleral wound implies an
As discussed previously, a contusive force entry into and through the sclera. However, since
introduced by a blunt object that induces a full- the eyewall is not used as a frame of reference
thickness defect is a rupture. Conversely, a sharp one cannot tell whether a globe laceration or an
object that induces a full-thickness defect is a IOFB is present. This could easily be a source of
laceration, but needs further distinction. Three confusion and misunderstanding that can lead to
possibilities exist: further miscommunication between healthcare
1. The entry and exit wound is the same: pene- professionals and to inappropriate or unneces-
trating injury (Figure 4.3A). sary evaluations. However, when the eyewall is
2. Separate entry and exit wounds caused by the used, this confusing situation is avoided and
same object are present: perforating injury tissue-specific terms are used only to locate the
(Figure 4.3B). entry wounds.
3. An entry wound is present and the object (or
a portion thereof) remains within the eye:
intraocular foreign body (Figure 4.3C).
Example 2
A referring doctor tells you that a patient has a scleral laceration.
The term ‘scleral laceration’ alone should not be used because of the confusion it creates.
The implication is that a sharp object has created a full-thickness defect in the sclera. However,
more information is mandatory so appropriate work-up and triage of the patient can be accom-
plished. If the laceration is into but not through the sclera, it should be referred to as a lamellar
laceration (a closed globe injury). Lamellar lacerations seldom require further ancillary testing
and can be transferred immediately. However, if the laceration is full thickness, it should be
referred to as a penetrating (open globe) injury. Further specification of the entry site is then
invaluable (i.e. scleral entry wound present 3 mm posterior to the limbus at 2 o’clock extend-
ing posteriorly approximately 2 mm). Depending on the mechanism of injury, further testing
(e.g. CT scan) is often necessary, typically before the patient is transferred, to determine
whether an intraocular foreign body is present. This example again illustrates the need for a
uniform terminology and classification scheme.
As is often the case, not all ‘real world’ injuries cause a ruptured globe and be retained as an
will fall nicely into one of the described catego- intraocular foreign body. Blast injuries can some-
ries. A blunt projectile with enough velocity can times create penetrating wounds, perforating
45
Ocular trauma
Table 4.2 Open globe injury classification.
Open globe injury classification

Type
A. Rupture
B. Penetrating
C. Intraocular
D. Perforating
E. Mixed
Grade
Visual acuity*
1. ≥20/40
2. 20/50 to 20/100
3. 19/100 to 5/200
4. 4/200 to light perception
5. No light perception†
Pupil
Positive: relative afferent pupillary defect present in affected eye
Negative: relative afferent papillary defect absent in affected eye
Zone
I: Isolated to cornea (including the corneoscleral limbus)
II: Corneoscleral limbus to a point 5 mm posterior into the sclera
III: Posterior to the anterior 5 mm of sclera
*Measured at distance (20 ft, 6 m) using Snellen chart or Rosenbaum near card, with correction and pinhole
when appropriate.
†
Confirmed with bright light source and fellow eye well occluded.
(From The Ocular Trauma Classification Group. A system for classifying mechanical injuries of the eye (globe).
Am J Ophthalmol 1997;128:820–831, with permission of Elsevier.)
wounds, and intraocular foreign bodies. These 4.2) and closed (Table 4.3) globe injuries. Injuries
sometimes are referred to as mixed-mechanism due to chemical, thermal, or electrical agents are
injuries. Nevertheless, these exceptions aside, not included in the classification. A recent study
the vast majority of injuries can be easily classi- showed that all four variables were significant in
fied and related to other healthcare professionals predicting fi nal visual outcome following open
in a uniform fashion. globe injury, although grade (visual acuity) and
pupil (presence of a relative afferent pupillary
CLASSIFICATION defect) were the most significantly predictive.5
A clinical classification system for mechanical PROGNOSIS AND PREOPERATIVE

eye injuries was developed in 1997 utilizing COUNSELING
the standardized ocular trauma terminology.3
The clinical variables were chosen because of Facing a potentially sight-threatening eye injury
their known prognostic significance. Indepen- is a harrowing ordeal for patients and their fami-
dent classifications are present for open (Table lies. Vision is often taken for granted, and the
46
Table 4.3 Closed globe injury classification.
Closed globe injury classification

Type
A. Contusion
B. Lamellar laceration
C. Superficial foreign body
D. Mixed
Grade
Visual acuity*
6. ≥20/40
7. 20/50 to 20/100
8. 19/100 to 5/200
9. 4/200 to light perception
10. No light perception†
Pupil
Positive: relative afferent pupillary defect present in affected eye
Negative: relative afferent papillary defect absent in affected eye
Zone‡
I: external (limited to bulbar conjunctiva, sclera, cornea)
II: anterior segment (involving structures in anterior segment internal to the cornea and including the
posterior lens capsule; also includes pars plicata but not pars plana)
III: posterior segment (all internal structures posterior to the posterior lens capsule)
*Measured at distance (20 ft, 6 m) using Snellen chart or Rosenbaum near card, with correction and pinhole
when appropriate.
†
Confirmed with bright light source and fellow eye well occluded.
‡
Requires B-scan ultrasonography when media opacity precludes assessment of more posterior structures.
(From The Ocular Trauma Classification Group. A system for classifying mechanical injuries of the eye (globe).
Am J Ophthalmol 1997;128:820–831, with permission of Elsevier.)
sudden nature of most traumatic eye injuries poor prognostic indicators for fi nal visual acuity
makes for a difficult situation. A question that outcomes. In the largest study to date, Kuhn
often occurs is ‘Will I go blind?’ or ‘Will my et al in 20029 analyzed over 2500 eye injuries.
vision recover?’ Through statistical analysis, six variables were
Being able to give a logical, scientifically based found to be of prognostic significance, and each
prognostication based on the initial examination variable was then assigned a point value (Table
allows the physician to counsel a patient and the 4.4). The mathematical sum of the given vari-
patient’s family objectively. Numerous studies ables is then broken into five categories (Table
have examined factors influencing fi nal visual 4.5) and allows the physician to estimate the
acuity following severe ocular trauma.6–8 Poor given probability of a certain level of visual
preoperative visual acuity, presence of a relative acuity recovery. This system is referred to as the
afferent pupillary defect, retinal detachment, Ocular Trauma Score (OTS) and can be posted
and large scleral lacerations were found to be in an examination area for quick reference.
47
Ocular trauma
Table 4.4 Calculating the OTS: variables and raw points.
Calculating the OTS: variables and raw points
Variable Raw points
Initial vision
NLP 60
LP/HM 70
1/200–19/200 80
20/200–20/50 90
≥20/40 100
Rupture −23
Endophthalmitis −17
Perforating injury −14
Retinal detachment −11
Afferent pupillary defect −10
(From Kuhn F, Maisiak R, Mann L et al. The ocular trauma score (OTS).
Ophthalmol Clin N Am 2002;15:163–165, with permission of Elsevier.)
Table 4.5 Calculating the OTS: categorization and potential visual acuity outcomes.
Calculating the OTS: conversion of raw points into an OTS category, and calculating the
likelihood of the final visual acuity in five categories
Sum of OTS No light Light 1/200–19/200 20/200–20/50 ≥20/40

raw points perception perception/
hand motion
0–44 1 74% 15% 7% 3% 1%

45–65 2 27% 26% 18% 15% 15%
66–80 3 2% 11% 15% 31% 41%
81–91 4 1% 2% 3% 22% 73%
92–100 5 0% 1% 1% 5% 94%
(From Kuhn F, Maisiak R, Mann L et al. The ocular trauma score (OTS). Ophthalmol Clin N Am 2002;15:163–165,
with permission of Elsevier.)
The road to recovery in severe ocular trauma sis of the severely injured eye while maintaining
is long and fraught with multiple surgeries and guarded optimism.
possible complications. Never downplay the sever- Anger and sadness are common reactions in
ity of the injury or the possibility for permanent loss the patient with a severely injured eye. Honesty
of sight. Be realistic when discussing the progno- and straightforward communication fosters a
48
trust between the patient and physician. Insist assure them all steps are being taken to restore
the patient be involved in the decision-making sight.
process. The Ocular Trauma Score is a spring-
board for answering difficult questions, but per- REFERENCES
sonal experience and common sense should
facilitate an honest conversation and a good rela- 1. Kuhn F, Morris R, Witherspoon CD, Heimann K, Jeffers JB,
tionship between patient and physician. My per- Treister G. A standardized classification of ocular trauma.
sonal experience has been that these patients are Ophthalmology 1996;103:240–243.
often some of the most loyal and grateful patients, 2. Kuhn F, Morris R, Witherspoon CD, Heimann K, Jeffers JB,
Treister G. A standardized classification of ocular trauma.
even when their visual outcomes are poor. If the
Graefe’s Arch Clin Exp Ophthalmol 1996;234:399–403.
patient realizes that all steps are being made to
3. Pieramici DJ, Sternberg P Jr., Aaberg TM Sr., et al. A system of
restore vision, their reaction to the physician and classifying mechanical injuries of the eye (globe). Am J
ancillary staff is typically one of gratitude, Ophthalmol 1997;123:820–831.
although their reaction to the situation may 4. Kuhn F, Morris R, Witherspoon CD. Birmingham Eye Trauma
often remain negative. Terminology (BETT): terminology and classification of
mechanical eye injuries. Ophthalmol Clin North Am
2002;15(2):139–143.
SUMMARY 5. Pieramici DJ, Au Eong KG, Sternberg P Jr., Marsh MJ.
The prognostic significance of a system for classifying
1. Strict adherence to the accepted ocular mechanical injuries of the eye (globe) in open-globe
traumatology defi nitions (Birmingham Eye injuries. Journal of Trauma-Injury, Infection and Critical
Trauma Terminology or BETT) is vital when Care 2003;54:750–754.
6. Hutton WL, Guller DG. Factors influencing final visual
assessing patients with eye injuries and when
results in severely injured eyes. Am J Ophthalmol 1984;97:
relaying information to eye care professionals.
715–722.
Only when these components are fully inte- 7. Abu El-Asrar AM, Al-Amro SA, Khan NM, Dangave D. Visual
grated into the vocabularies and methodo- outcome and prognostic factors after vitrectomy for
logies of physicians caring for this population posterior segment foreign bodies. Eur J Ophthalmol
of patients can effective communication and 2000;10:304–311.
8. De Souza S, Howcroft MJ. Management of posterior segment
reliable triage of patients be accomplished.
intraocular foreign bodies: 14 years’ experience. Can J
2. Establishing an honest, therapeutic relation-
Ophthalmol 1999;34:23–29.
ship with the patient is of utmost importance 9. Kuhn F, Maisiak R, Mann L, Mester V, Morris R, Witherspoon
when facing a severe ocular injury. Involve the CD. The Ocular Trauma Score. Ophthalmol Clin N Am
patient in the decision-making process and 2002;15:163–165.
49
5
Closed globe injuries: ocular surface
(conjunctiva, cornea, and sclera)
Kristen L. Hartley, Benjamin L. Mason, James T. Banta
INTRODUCTION proceed in a stepwise fashion. History is critical

in determining the mechanism of injury. In par-
Closed globe injuries to the conjunctiva, sclera, ticular, the patient’s activities at the time of
and cornea are commonplace and are a frequent injury, the injuring agent, subsequent vision loss,
reason emergency ocular care is sought. When prior treatments, and current level of discomfort
the eyes are open, the ocular surface (particu- should be thoroughly documented. However,
larly the epithelium of the cornea and conjunc- thorough history taking in the setting of chemi-
tiva) acts as a protective barrier to the elements. cal injuries should initially be avoided so that
The majority of ocular surface injuries occur immediate and copious irrigation of the eye can
when a foreign substance or object inadvertently begin.
(job-related accident) or purposefully (assault) The upper and lower conjunctival fornices are
comes into contact with the ocular surface. formed at the transition between tarsal and
Depending on the mechanism of injury, these bulbar conjunctiva (Figure 5.1). The fornices can
injuries vary from mild (subconjunctival hemor- harbor unrealized foreign material or retained
rhage) to vision threatening (alkali exposure). chemicals. The upper lid should be everted to
While most surface injuries are benign and examine the tarsal conjunctiva and, in appropri-
resolve without intervention, others require close ate cases, ‘double eversion’ of the eyelid is per-
inspection and prompt treatment to prevent performed to thoroughly examine the upper fornix
manent dysfunction or late complications. Com- (see Chapter 3).
placency is ill advised as a seemingly innocuous The ocular examination will vary depending
injury can sometimes herald more serious pathol- on the mechanism of injury. An initial inspec-
ogy. A comprehensive examination is necessary tion is made to ascertain the integrity of the
for even a seemingly minor injury. In this chapter eyewall. Once an open globe injury has been
we will review common traumatic injuries to the excluded, a thorough examination of the ante-
ocular surface. rior segment with special attention to the forni-
ces is carried out. The pH of the eye should be
measured with any chemical injury. The tarsal
EVALUATION: GENERAL and bulbar conjunctiva should be examined for
CONSIDERATIONS presence of hemorrhage, foreign material, edema,
subconjunctival air, or lacerations. The cornea
Injuries to the ocular surface encompass a vast should be examined for the presence of epithe-
array of diagnoses. Although the specific history lial defects, foreign bodies, lamellar lacerations,
and examination fi ndings for each diagnostic or limbal stem cell ischemia. The sclera should
entity will be described individually, the evalua- also be examined for lamellar lacerations, foreign
tion for injuries of the ocular surface should bodies, and structural integrity.
51
Ocular trauma
Superior
conjunctival
fornix
Figure 5.2 Subconjunctival hemorrhage associated

Inferior with an open globe is often present 360 degrees and
conjunctival associated with chemosis. This 42-year-old female
suffered a severe contusive trauma to the left eye and
fornix
was found to have a large posterior rupture during
surgical exploration.
viral conjunctivitis is also a common cause. Sys-

Figure 5.1 The tarsal conjunctiva (red) begins at the temic hypertension and anticoagulation can pre-
posterior edge of the eyelid margin and is tightly dispose patients to more frequent hemorrhages.1,2
adherent to the underlying tarsal plate. The palpebral Frequently, no specific cause is elucidated.
conjunctiva (blue) inserts at the limbus, is more mobile Traumatic subconjunctival hemorrhage can be
and overlies Tenon’s capsule. The superior and inferior
related to trauma as minor as excessive eye
conjunctival fornices form at the transition between
rubbing or as extreme as open globe injuries.
the tarsal and palpebral conjunctiva.
Evaluation
TRAUMATIC SUBCONJUNCTIVAL History is the most important step in determin-
HEMORRHAGE ing the etiology of a subconjunctival hemorrhage.
Subconjunctival hemorrhage often obscures the
Introduction underlying sclera so eliciting the exact mecha-
Subconjunctival hemorrhage is a very common nism of injury can help the examiner determine
condition that presents as an ocular emergency, the risk of severe ocular damage. Occult globe
in large part due to its often dramatic appear- violation can be masked by the presence of dense
ance. The causes of subconjunctival hemorrhages subconjunctival hemorrhage and requires a high
are numerous and the severity can be variable. index of suspicion to diagnose (Figure 5.2).
Spontaneous subconjunctival hemorrhage is Careful examination technique can typically
frequently due to Valsalva maneuvers that raise detect the presence or absence of an occult globe
venous pressure such as coughing, sneezing, violation in the setting of dense subconjunctival
vomiting, or heavy lifting. Acute bacterial or hemorrhage. Examination clues include:
52
Closed globe injuries: ocular surface (conjunctiva, cornea, and sclera)
1. peaked pupil the mechanism of injury is important as it helps

2. asymmetric anterior chamber depth determine the risk of infection or retained foreign
3. asymmetrically low intraocular pressure body.
4. subconjunctival pigment A corneal abrasion can be hard to see at the slit
Chapter 11 explores the diagnosis of occult globe lamp unless the loose epithelium is heaped up
violation in further detail. and incompletely avulsed from the underlying
stroma. Fluorescein staining of the cornea is the
Treatment mainstay of diagnosis. When the epithelial defect
Recognizing and treating any associated ocular is stained, the affected area can easily be visual-
injuries is the fi rst and most important step. The ized and measured. The areas without epithe-
only treatment for subconjunctival hemorrhage lium take up the fluorescein and turn bright
is time. Most subconjunctival hemorrhages green under examination with a cobalt blue fi lter
resolve in a matter of days but can take several (Figure 5.3). Documenting the horizontal and
weeks if extensive. Conservative measures vertical size of the defect can be helpful in moni-
such as lubricant eye drops and reassurance are toring a patient’s recovery.
satisfactory with isolated subconjunctival Associated exam fi ndings may include subcon-
hemorrhages. junctival hemorrhage, conjunctival abrasions and
Patients with isolated subconjunctival hemor- lacerations, corneal stromal edema, Descemet’s
rhages can be followed on an as-needed basis folds (Figure 5.4), and anterior chamber cell and
assuming a routine recovery. Patients need to be flare. With very severe trauma a corneal abrasion
informed that the hemorrhage can initially may be seen with hyphema, commotio retinae,
expand in size and eventually change color over or even an open globe.
a 10–14-day course. If significant trauma led to Further exam is critical to rule out associated
the hemorrhage then follow-up is determined by conditions that can coexist with corneal
the severity of concomitant ocular injuries.
CORNEAL ABRASIONS
Introduction
Trauma to the cornea is an extremely common
cause of visits to an emergency center. Typically,
the corneal epithelium is torn away from the
underlying stroma by trauma from a foreign
object. Some of the most common reasons for
traumatic corneal abrasions include eye rubbing,
fi ngernail injuries, thrown objects, chemical
exposure, and contusive trauma (e.g. air bag
injury, 3 assault).
Evaluation Figure 5.3 A defect in the corneal epithelium is most

Patients typically present with intense pain, pho- easily observed utilizing fluorescein dye viewed with a
tophobia and redness. Careful questioning about cobalt blue light.
53
Ocular trauma
Figure 5.4 Descemet’s folds and mild stromal edema

are seen in association with a resolving corneal
abrasion (seen inferiorly).
B
abrasions. A careful examination of the unin-
volved corneal epithelium should be performed.
Underlying anterior basement membrane dystro-
phy (also known as map-dot-fi ngerprint dystro-
phy) is a common association.4,5 Patients with
this condition have a weakened epithelial adher-
ence and are prone to abrasions with minimal
trauma. Associated keratitis must also be ruled
out, and if found, appropriate cultures should be
obtained. A particularly high index of suspicion Figure 5.5 A 32-year-old male presented with pain and
for keratitis is needed if the corneal abrasion was foreign body sensation in the right eye. Slit lamp
caused by contact lenses or organic material (e.g. examination revealed vertically oriented linear corneal
tree branch). abrasions (A) prompting a search of the upper tarsal
conjunctiva (B). The foreign body was removed with a
Linear corneal abrasions, particularly when
cotton-tipped swab.
oriented vertically, are a tell-tale sign of subtarsal
Included
on DVD foreign bodies (Figure 5.5). Everting the upper
eyelid and sweeping the conjunctival fornices are treated as a routine corneal abrasion (see below).
helpful techniques to fi nd and remove residual The patient is then re-evaluated a day or two
particulate matter. later. If the dendritic appearance is unchanged
As corneal epithelial defects heal, they often or worse, a presumptive diagnosis of herpetic
take on a dendritic appearance which can some- disease can be made and appropriate work-up
times be confused with herpetic disease (Figure and management can be initiated.
5.6). History and timeline play a vital role in
differentiating the two diagnoses. Corneal abra- Treatment
sions, particularly smaller ones, heal in a matter Loose or heaped up epithelium should be
of hours. If any question exists, the lesion can be debrided to encourage re-epithelialization. Even
54
most corneal abrasions. Patient preference can

help determine the choice between ointments
and drops. Eye drops are simple to use and do
not further blur the vision. Ointments offer an
additional lubricating effect that increases
comfort but also causes significant blurring. A
course of 3–5 days should suffice for most abra-
sions. Specific instructions are given to avoid eye
rubbing.
Significant controversy surrounds the use of
adjuvant occlusive patches for corneal abrasions.
Figure 5.6 As the corneal epithelium heals, a pseudo-
dendritic appearance is sometimes seen in the final Studies have shown that occlusive patching does
stages of healing. not significantly speed corneal re-epithelializa-
tion or improve patient comfort.6,7 Furthermore,
if a partially avulsed flap of corneal epithelium the fear of possibly accelerating infection has
can be temporarily replaced this should be tempered the use of patching in recent years. In
avoided. With repeated blinking the loose epi- the absence of apparent infection, the authors
thelium will again become dislodged and may prefer to utilize an antibiotic ointment (bacitra-
hinder the healing process and contribute to cin or erythromycin ointment) without occlusive
patient discomfort. A moistened sterile swab can patching. In the rare instances we use occlusive
be used to debride a partially avulsed epithelial patches, we patch only if the wound is consid-
flap, but use of a sharp blade to remove heaped- ered low risk (no history of contact lens use or
up edges or large sheets of loose epithelium is exposure to organic material) and pain is seem-
preferred as it is less likely to propagate the ingly uncontrollable. This is only done if the
defect into normal epithelium. patient is deemed reliable and agrees to follow-
One of the keys to treatment success is removal up the following day. Never patch an eye that has
of any residual foreign material. The upper lid an abrasion associated with contact lenses or
should be everted and the tarsal conjunctiva organic material.
should be examined for foreign bodies. The In the presence of a suspected infectious kera-
conjunctival fornices should be swept if the titis, corneal scrapings are obtained and sent for
potential for foreign material exists. This is ac- Gram stain and culture. Our initial antibiotic
complished after applying topical anesthetic to choice depends on the location and size of the
the eye. A moistened cotton swab or glass rod is infi ltrate. For a small peripheral infi ltrate, the
introduced into the conjunctival fornix (both authors prefer a fourth-generation fluoroquino-
superior and inferior) and is moved along the lone used hourly. If the infi ltrate is large or
entire length of the forniceal space. If debris is threatening the visual axis, fortified cefazolin
encountered, the procedure should be repeated and tobramycin are prescribed and used hourly.
until no foreign material is seen. Corneal or con- Antibiotic use is then tailored to the culture
junctival foreign bodies should likewise be results.
removed (see below). Pain is a significant issue with corneal abra-
Prophylactic broad-spectrum antibiotics and sions. Fortunately, in routine cases, the rapidity
observation are the mainstays of treatment for with which the corneal epithelium regenerates
55
Ocular trauma
causes the painful episode to be relatively short- anesthetic drop gives a ‘miraculous’ reprieve
lived. Abrasions located within the intrapal- from the pain often leaving the patient incredu-
pebral space are more symptomatic as blinking lous when they are told it cannot be used rou-
causes contact with the injured epithelium. Con- tinely. Chronic use of topical anesthetics retards
versely, abrasions located in the superior aspects wound healing and can lead to severe corneal
of the cornea tend to be better tolerated since complications such as corneal melting.8 The
the upper lid covers and protects them. We rou- authors have seen patients attempt to steal
tinely counsel patients on the expected discom- topical anesthetic bottles from the examination
fort as the abrasion heals. If the abrasion is small room. We have also seen topical anesthetics inap-
or the patient is pain-tolerant, acetaminophen propriately prescribed by non-ophthalmologists.
taken regularly during the acute phase is recom- Healthcare providers (including veterinarians)
mended. Acetaminophen should be avoided in are a high-risk group for anesthetic abuse since
patients with liver dysfunction and recom- they often have access to the medicines but are
mended dosages should be followed closely. If not always aware of its associated dangers. Spe-
the patient is in severe pain, as is often the case, cific counseling as to why the anesthetic drops
a prescription for a 2-day supply of narcotic anal- are not a part of treatment is recommended, and
gesics is given. anesthetic bottles need to be accounted for at the
end of each examination. Deterioration of the
Complications and outcomes cornea following a corneal abrasion should spur
Patients who are patched should be examined an inquiry about the inappropriate use of topical
within 24 hours. Non-patched small abrasions anesthetics.
can be given antibiotic coverage for 3–5 days
with follow-up scheduled on an as-needed basis. CORNEAL FOREIGN BODIES
For large abrasions the healing process should be
evaluated in 1–2 days. If signs of infection are Introduction
present or if the abrasion is considered high risk Corneal foreign bodies are one of the most
for infection, daily follow-up is warranted until common forms of ocular trauma, second only to
healing is complete. corneal abrasions.9 It is of utmost importance
Changes in corneal epithelial adherence can that each patient presenting with a corneal
occur following a traumatic corneal abrasion. foreign body be educated on the use of protec-
This can lead to recurrent corneal erosions in the tive eyewear, as this could prevent most com-
absence of significant trauma.4 These patients monly encountered corneal foreign body injuries
often report a history of waking from sleep with (see Chapter 2). Most corneal foreign bodies are
severe eye pain that may resolve over the next not associated with a high level of morbidity, but
few hours. If the problem is recalcitrant despite it is essential to perform a thorough examina-
appropriate lubricant use, referral to an anterior tion, including a dilated fundus examination, to
segment specialist is warranted, as various thera- rule out an intraocular foreign body.
peutic modalities are available (stromal punc-
ture, therapeutic keratectomy). Etiology
The use and abuse of anesthetic drops deserves The causes of corneal foreign body injuries are
special mention. The pain from corneal abra- numerous. Injury may occur to the unassuming
sions can be intense. The placement of a topical individual who has debris blown into the eye
56
while driving or walking down the street.

However, most corneal foreign body injuries are
related to lack of protective eyewear while per-
forming high-risk activities such as grinding,
drilling, hammering, and welding. 9
Evaluation
A thorough history and full ophthalmic evalua-
tion are crucial in a patient presenting with a
corneal foreign body, and the possibility of an
open globe injury and an intraocular foreign
body needs to be fully excluded. A thorough
Figure 5.7 A metallic corneal foreign body is
history will lower (e.g. something fell into the
embedded in the nasal aspect of the cornea in a 26-
eye while walking down the street) or raise year-old male patient who suffered the injury while
(e.g. hammering metal on metal) the suspicion grinding metal without appropriate eye protection.
of a more serious injury. After obtaining a history,
full ophthalmic examination should be per-
formed. Visual acuity is an essential piece of foreign body is present. The cornea should fi rst
information and if decreased should raise the be evaluated with a wide beam and then a slit
suspicion for a more serious injury. An initial beam to determine the depth of a corneal foreign
screening slit lamp examination should be per- body. The location and properties (metallic or
formed to confi rm that no globe violation has non-metallic) of the foreign body should be doc-
occurred. Carefully document intraocular pres- umented. If the foreign body is in the posterior
sure in both the affected and unaffected eye. portion of the corneal stroma, perform a Seidel
Asymmetric intraocular pressure readings may test over the area of the foreign body before and
be an early clue that the integrity of the globe after removal to rule out egress of aqueous from
has been compromised. Full slit lamp examina- the wound. The anterior chamber should be
tion should begin with evaluation of the patient’s evaluated thoroughly, including depth of the
lids and lashes. Evert the upper lids and evaluate chamber, amount of anterior chamber reaction,
both the upper and lower tarsal conjunctiva and and evidence of hyphema or hypopyon. The iris
fornices for any evidence of retained foreign should be evaluated for the presence of trans-
bodies. Vertically oriented linear corneal abra- illumination defects and the lens for evidence
sions often coexist with subtarsal foreign bodies of anterior lens capsule disruption, intralenticu-
and are easily seen with fluorescein staining. lar foreign body, or cataractous changes. Finally,
Conjunctival chemosis should raise the suspicion a dilated fundoscopic examination should be
for a globe violation if present. The bulbar con- performed if an intraocular foreign body is a
junctiva should be thoroughly inspected for lac- possibility.
erations, foreign bodies, or debris.
Often a corneal foreign body is quite obvious Treatment
(Figure 5.7). It is of paramount importance to Most corneal foreign bodies are metal and can
continue looking for other foreign bodies or con- be removed easily at the slit lamp. Shallow
comitant ocular injuries even when an obvious foreign bodies often can be dislodged with a
57
Ocular trauma
moistened sterile cotton swab. Embedded foreign the eye to prevent inadvertent eye rubbing. A
bodies can be removed with a small gauge needle topical aqueous suppressant is sometimes pre-
(27- or 30-gauge), ophthalmic ‘spud,’ rotating scribed to decrease the flow of aqueous through
ophthalmic burr, or a combination of the three. the wound thereby encouraging wound healing.
In the case of a metallic foreign body, it is impor- Daily follow-up is mandatory in these cases.
tant to remove any associated rust ring to prevent Deep foreign bodies consisting of an inert
a secondary keratitis. The following steps are substance (e.g. glass, plastic) are sometimes
used when removing a corneal foreign body: left in place to be serially observed. Foreign
1. Anesthetize the eye. bodies will sometimes slowly migrate anteriorly
2. Insert a lid speculum (if the patient has diffi- with time allowing for a safer, more controlled
culty keeping the eye open). removal.
3. Place the patient in the slit lamp and locate
the foreign body (Figure 5.8A). Complications and outcomes
4. Using a needle, approach the cornea tangen- Follow-up should be tailored to each individual
Included
tially so that no sudden movement could lead patient. If the corneal foreign body is small and
on DVD
to perforation of the anterior chamber. leaves only a small corneal epithelial defect and
5. Gently dislodge the foreign body and remove no rust ring after removal, the patient may be
it from the surface of the eye (Figure 5.8B). seen on an as-needed basis. In the case of a large
6. If metallic, the foreign body typically leaves a corneal foreign body with a large epithelial defect
rust ring in place which is removed with an after foreign body removal, the patient should be
ophthalmic corneal burr (Figure 5.8C) until followed daily to be sure the abrasion is healing
the ring is entirely removed (Figure 5.8D). with no evidence of secondary infection. If a rust
7. After the foreign body has been removed, the ring is still present at discharge, the patient
patient should be placed on an antibiotic oint- should be followed daily with continued attempts
ment (e.g., bacitracin or erythromycin) four to remove all rust from the cornea. In many
times daily and a cycloplegic, if necessary. cases, the rust is more easily removed after 1–2
8. Counseling on the necessity for protective days of observation. All patients should be
safety goggles during high-risk activities is instructed to return immediately if symptoms
vital as recurrences are common with metallic worsen (e.g. decreased vision, increased pain or
corneal foreign bodies. redness).
Deeply embedded foreign bodies can be quite
challenging to manage. When the foreign body
is greater than 80% depth, it is possible that CHEMICAL INJURIES
removal may create a small full-thickness corneal
injury. If removal is attempted, a Seidel test Introduction
should be performed immediately afterwards. If Chemical injuries are true ocular emergencies.
positive, a decision to use corneal glue or a suture Every second counts after a chemical injury since
will need to be made. Most small-caliber wound the amount of tissue damage is directly related
leaks following foreign body removal will close to the length of time the chemical remains in
spontaneously in a matter of hours and can be contact with the eye. Immediate irrigation is
closely observed with the typical regimen of vital. Ideally, irrigation should begin long before
topical antibiotics and a protective shield over a patient’s presentation to the emergency room.
58
A B
C D
Figure 5.8A–D Metallic corneal foreign body removal.
Chemical composition is also important. Alka- into the anterior chamber may occur rapidly
line agents tend to penetrate the eye more readily after some alkali injuries (e.g. ammonia), further
than acids thereby carrying a significantly higher emphasizing the importance of immediate treat-
morbidity.10–12 ment.10–12 Education, particularly for high-risk
Depending on the depth of ocular penetration, individuals such as custodians and laboratory
a chemical injury may cause damage to many workers, is very important because they need to
ocular structures including the corneal and be aware that irrigation should be started at
conjunctival epithelium, basement membrane, home or in the field immediately after exposure.
corneal stroma and endothelium, lens epithe- Prevention with appropriate eye protection could
lium, and vascular endothelium of the conjunc- prevent most, if not all, chemical injuries in
tiva, episclera, iris, and ciliary body.11 Penetration working environments.
59
Ocular trauma
Figure 5.9 Diffuse conjunctival ischemia, corneal haze, Figure 5.10 Moderate conjunctival injection with a
and a sterile inflammatory hypopyon are seen central corneal epithelial defect following exposure to
following a severe alkali exposure. an acidic compound during a splash injury at work. The
conjunctival injection, particularly at the limbus is a
good indication of limbal stem cell viability.
Pathophysiology
As stated previously, chemical injuries may be (Figure 5.11).11 This can be an arduous, messy
associated with either acid or alkali compounds. process that can sometimes take over an hour,
Alkalis cause the most severe damage by dis- but it is essential to minimize further damage to
rupting the corneal barrier and allowing rapid the eye.10,13,14 To achieve complete irrigation of
passage into more posterior ocular structures. the conjunctival fornices, it is often necessary
Lye (NaOH, KOH), fresh lime (CaO, found in to apply topical anesthetic (e.g. tetracaine or
plaster and concrete), and ammonia are the most proparacaine) and retract the lids with a lid
commonly involved agents.10,11 Alkalis result in a speculum or Desmarres retractor.15 Irrigation is
more severe injury as they rapidly penetrate the complete when the pH of the eye has normalized
eye, saponify cell membranes, denature collagen, and all foreign material has been removed. While
and thrombose vessels (Figure 5.9).12 Intraocular irrigation is being performed, a thorough history
pressure may be elevated initially due to shrink- should be obtained to determine the type of
age of the scleral collagen and later by sclerosis chemical involved. If a sample of the chemical is
of the aqueous outflow channels.11–13 Acids gen- available, pH testing should be performed
erally cause less damage because the hydrogen directly on the sample.
ion precipitates protein and prevents further Once irrigation is complete, a more compre-
penetration through the cornea (Figure 5.10).12 hensive examination is performed. Vision and
However, treatment and potential complications pressure should be documented, as the pressure
are similar for both alkali and acid injuries. may be acutely elevated. Attention is then focused
on the anterior segment. The lids and lashes are
Evaluation evaluated to look for any evidence of crystallized
Obtaining an initial history of chemical expo- chemicals. These are removed immediately if
sure is all that is necessary before immediate, present. The upper and lower conjunctival for-
copious irrigation with liter bags of normal saline nices should be swept with a glass rod or sterile
is initiated. The eye should be irrigated with cotton swab to remove any offending agents.
normal saline until the pH of the eye normalizes A careful examination of the conjunctiva and
60
Figure 5.11 Following a chemical injury, immediate Figure 5.12 Severe conjunctival and limbal ischemia
copious irrigation of the involved eye is initiated with following an alkali injury. Notice the pruning of the
liter bags of normal saline. remaining conjunctival vessels.
cornea should be performed. The Roper-Hall Treatment

modification of the Hughes classification system Initial management, as mentioned previously,
is a widely accepted guide for the standardized involves copious irrigation and meticulous
assessment and prognosis of chemical burns:16 removal of all chemical residues. Irrigation is
1. Grade 1: epithelial damage with no limbal typically performed with the patient lying at an
ischemia angle, allowing the excess water to be collected
2. Grade 2: corneal haze, visible iris details, and in a basin. Retractors are used to make certain
ischemia less than one-third of the limbus the fluid reaches the conjunctival fornices. This
3. Grade 3: total loss of corneal epithelium, is continued until the pH of the eye normalizes.
stromal haze obscuring iris details, and is- Successful long-term management of chemical
chemia of one-third to one-half of the limbus burns involves promoting re-epithelialization,
4. Grade 4: opacified cornea, iris and pupil minimizing inflammation, and reducing the inci-
obscured, and ischemia involving more than dence of corneal perforation. The management
half of the limbus. of chemical injuries is dependent on the degree
The size of the corneal epithelial defect should of ocular injury. In the case of a Grade 1 injury,
be well documented as well as the clock hours the patient should be treated with an antibiotic
of limbal ischemia, if present. Limbal ischemia ointment (e.g. bacitracin or erythromycin) four
appears as a blanching of normal limbal vessels times daily to the affected eye and a cycloplegic
(Figure 5.12). A white eye in the setting of a (e.g. scopolamine) to decrease ciliary spasm and
chemical injury is a very poor prognostic indica- decrease the formation of posterior synechiae.12
tor and indicates diffuse vascular damage. Ante- One can also consider the use of topical steroids
rior chamber reaction should be documented as (e.g. prednisolone acetate) to decrease the
this can provide indirect evidence of intraocular inflammatory response for the fi rst 7–10 days
chemical penetration. after injury.11–14 Topical steroids should be rapidly
61
Ocular trauma
tapered after that time due to the risk of impaired adrenergic agonists (e.g. brimonidine), or carbonic
wound healing with long-term use. In more anhydrase inhibitors (e.g. dorzolamide).11–13
severe injuries, high-dose vitamin C (500 mg
orally four times a day), 10% ascorbate drops Complications and outcomes
every 2 hours, and 10% citrate drops every 2 The patient should be followed on a daily basis
hours were associated with a more rapid recov- to ensure the treatment regimen is leading to
ery and better fi nal visual outcome in one study.17 clinical improvement. In severe cases with limbal
Oral doxycycline (50–100 mg orally two times ischemia or intraocular complications, daily
a day) is a potent inhibitor of collagenase and visits are essential to monitor for evidence of
may reduce the risk of corneal perforation in a corneal thinning or perforation. Rarely, immedi-
severely injured eye.18 ate surgical treatment with a temporary tarsor-
Intraocular pressure in a chemically injured eye rhaphy, corneal glue, or if these more conservative
may be high or low. Decreased pressure is usually measures fail, an emergent corneal patch graft or
due to ciliary body damage. A high IOP is most corneal transplant is necessary when perforation
likely caused by collagen shrinkage or inflam- occurs or is imminent. Consultation with an
matory debris obstructing the trabecular mesh- anterior segment specialist is often necessary for
work.11–13 Control of IOP is best achieved with long-term management, particularly when limbal
aqueous suppressants, such as topical beta- stem cell ischemia is present and/or anterior
adrenergic antagonists (e.g. timolol), alpha- segment reconstruction is necessary.
CASE EXAMPLES
Case report: chemical injury (Figure 5.13)

A 48-year-old male was working when a car battery returned 3 days later with reports of improved
(sulfuric acid) exploded in his face. He immediately comfort and vision. Visual acuity improved to 20/60.
flushed the eyes with water but noted severe Slit lamp examination revealed a central clear
decrease in visual acuity associated with severe pain zone devoid of epithelium. The peripheral cornea
in both eyes. Initial visual acuity was counting fingers remained opaque with significant white blood cell
in both eyes. Slit lamp examination of the right eye infiltrate (B). Treatment was continued and the
revealed extensive conjunctival ischemia with limbal patient slowly improved. Follow-up 17 days after the
vessels present only superiorly. Extensive superficial initial injury showed dramatic improvement in con-
necrosis and white blood cell infiltration of the junctival vascularization associated with clearing
cornea obscured the view of anterior chamber struc- and re-epithelialization of the peripheral cornea. A
tures, although the anterior chamber did appear to small central epithelial defect persisted (C). Four
be formed (A). The left eye suffered only a small weeks after the initial injury, the cornea was com-
central epithelial defect and will not be discussed pletely re-epithelialized with a mild anterior stromal
further. The patient was started on an antibiotic oint- haze (D). Best corrected visual acuity was 20/50.
ment, cycloplegic drops, and topical steroids. He
62
Case report: chemical injury (cont’d)
A B
C D
CONJUNCTIVAL LACERATIONS
Introduction
Conjunctival lacerations are often caused by
foreign body trauma. One very frequent cause is
inadvertent fi ngernail injury, often caused by
small children inadvertently striking caretakers
or between adults during sporting events (Figure
5.14). Machine workers and other fabrication
and construction workers are also considered
high-risk.
Evaluation Figure 5.14 A 22-year-old male was accidentally poked

Patients often complain of a foreign body sensa- in the eye while playing basketball. A stellate, 12 mm
conjunctival laceration was present temporally. Since
tion and tearing. A history consistent with a
the laceration was largely protected by the lids, the
foreign body injury such as inadvertently being patient experienced minimal discomfort and the
poked in the eye is typically elucidated. The laceration healed without suturing.
nature of the injury can help one develop an
63
Ocular trauma
initial assessment of the patient’s risk of globe lacerations should often be sutured. A horizon-
violation and infection. tally oriented laceration often comes in contact
Examination should consist of a complete with the lid margin during blinking, thus pro-
ocular examination including a dilated fundus longing healing time and increasing foreign body
examination to rule out a more serious injury. sensation. Large and/or poorly approximated
Special attention is given to the area of the lac- wounds will often eventually heal without inter-
eration. Fluorescein can help determine the size vention but can leave scar tissue and produce a
of the laceration. If the underlying sclera is lacer- chronic foreign body sensation. Absorbable
ated, a Seidel test should be performed at the suture such as polyglactic acid (7-0 or 8-0)
site to rule out an open globe injury (see Chapter should suffice to cover bare sclera and can be
3). Every conjunctival laceration should be done in a minor operating room or even at the
explored extensively under topical anesthesia. slit lamp. The authors prefer to close large con-
The length of laceration, the approximation of junctival lacerations if the approximation is poor
the wound edges, and the amount of debris and healing is likely to cause scarring if left unsu-
should be documented. Conjunctival chemosis tured. We employ multiple buried simple inter-
and surrounding subconjunctival hemorrhage rupted sutures to assure good closure and
can sometimes obscure foreign material and decrease the risk of wound dehiscence if a suture
scleral injury, so gentle probing with a cotton breaks.
swab can be useful under topical anesthesia.
Retained foreign bodies can increase a patient’s Complications and outcomes
risk of infection and persistent inflammation. Isolated small lacerations treated only with pro-
Rarely, pigmented uvea protruding through a phylactic antibiotics can be seen on an as-needed
full-thickness scleral laceration can be confused basis if their recovery is unremarkable. More
with a foreign body and requires careful exami- extensive or sutured lacerations should be re-
nation under a slit lamp to help differentiate evaluated in 5–7 days.
between the two entities.
Treatment
Once the integrity of the eyewall is confi rmed, LAMELLAR CORNEAL AND
cotton swabs, forceps, or saline irrigation can be SCLERAL LACERATIONS
used to remove persistent debris or residual
chemical residue. Most small conjunctival lacera- Introduction
tions can be treated conservatively with prophy- Lamellar or partial-thickness lacerations of the
lactic topical antibiotics for 5–7 days. Antibiotic cornea and sclera are relatively uncommon (aside
ointments are often utilized as their lubricating from metallic corneal foreign bodies discussed
properties contribute to the patient’s comfort, earlier). These injuries are often caused by
although topical drops will suffice. foreign body trauma with a sharp object such as
Some ophthalmologists advocate suturing all a screwdriver or pencil (Figure 5.15).
conjunctival lacerations. Most small lacerations
(<10 mm) will heal quickly without surgical Evaluation
intervention. Larger (>10 mm), poorly approxi- History is critical, particularly the mechanism of
mated, and horizontally oriented conjunctival injury. The injuring object should be identified,
64
A from the laceration site can sometimes reveal

low-grade flow through a small full-thickness
wound. A complete ocular examination to rule
out other injuries is important for any patient
who suffers significant eye trauma.
Treatment
Lamellar wounds can be at an increased risk of
infection, especially if the injury involved an
organic or ‘dirty’ object. Organisms can be
seeded deeply, making them somewhat more
B resistant to topical antibiotics. For this reason
the wound should be cleaned of any foreign
material and irrigated to help the healing process
and reduce the risk of infection. Broad-spectrum
topical antibiotics should be used as prophylaxis
until the wound is completely healed.
Deep lamellar wounds at risk for subsequent
rupture with minor trauma should be protected
with an eye shield. The shield should also be
worn at night to prevent inadvertent eye rubbing.
Suturing of lamellar wounds is rarely necessary
unless the length of the wound causes significant
gaping. Corneal glue is another treatment option
if the wound is limited to the cornea and more
defi nitive intervention is required.
Figure 5.15 A 42-year-old male was struck with a tile
fragment while cutting tiles without appropriate eye Complications and outcomes
protection. A horizontally oriented corneal laceration
Deep lamellar lacerations should be followed
was noted (A). Slit beam examination revealed the
laceration was approximately 80% depth (B). A Seidel
closely for signs of infection and to ensure wound
test was negative. A shield was placed over the eye and healing is adequate. Patients should be given spe-
the patient was placed on prophylactic antibiotic cific instructions about the symptoms of infec-
drops. Serial observation was elected, and the wound tion and instructed to return immediately if such
healed without sequelae. symptoms occur. Depending on the location and
depth of the wound, lamellar corneal lacerations
often leave a scar and can sometimes induce
if possible. A thorough examination of the irregular astigmatism.
injured area is then performed to confi rm that
the wound is indeed only partial thickness. A SUMMARY
Seidel test is of utmost importance. If a wound
is considered highly suspicious yet has an ini- 1. Injury to the ocular surface (particularly
tially negative test, light globe pressure away corneal abrasion) is the most commonly
65
Ocular trauma
encountered sequela following ocular 5. Brown NA, Byron AJ. Recurrent erosion of the cornea.
trauma. Br J Ophthalmol 1976;60:84–96.
6. Arbour JD, Brunette I, Boisjoly HM, Shi ZH, Dumas J, Guertin
2. Appropriate eye protection could prevent all
C. Should we patch corneal erosions? Arch Ophthalmol
on-the-job ocular surface injuries. 1997;115:313–317.
3. Traumatic subconjunctival hemorrhage has no 7. Kaiser PK. A comparison of pressure patching versus no
specific treatment, but should lead to an patching for corneal abrasions due to trauma or foreign body
appropriate examination to rule out concomi- removal. Corneal Abrasion Patching Study Group.
tant ocular injury. Ophthalmology 1995;102:1936–1942.
8. Rosenwasser GO. Complications of topical ocular anesthetics.
4. Corneal abrasions typically heal quickly and
Int Ophthalmol Clin 1989;29(3):153–158.
require only prophylactic antibiotics. Loose 9. Hamill MB. Corneal injury. In: Krachmer JH, Mannis MJ,
sheets of epithelium should be debrided to Holland EJ, eds. Cornea: Fundamentals of Cornea and
promote re-epithelialization. External Disease. Vol. 2. St. Louis: Mosby; 1997;1416–1419.
5. Metallic corneal foreign bodies and their asso- 10. Ralph RA. Chemical injuries of the eye. In: Tasman W, Jaeger
ciated rust rings should be completely removed EA, eds. Duane’s Clinical Ophthalmology. Vol. 4. Philadelphia:
Lippincott, Williams, and Wilkins; 1998:1–23.
to prevent keratitis. Occasionally, recalcitrant
11. Wagoner MD. Chemical injuries of the eye: current concepts
rust rings are left in place for 1–2 days (while in pathophysiology and therapy. Surv Ophthalmology
using a prophylactic antibiotic) since delayed 1997;41(4):275–313.
removal is often much easier to accomplish. 12. Yu JS, Ralph RA, Rubenstein JB. Ocular burns. In: MacCumber
6. Irrigation of chemical injuries should begin MW, ed. Management of Ocular Injuries and Emergencies.
before the patient arrives in the emergency Philadelphia: Lippincott-Raven; 1998:163–171.
13. Pfister DA, Pfister RR. Acid injuries of the eye. In: Krachmer JH,
room and again upon arrival at the emergency
Mannis MJ, Holland EJ, eds. Cornea: Fundamentals of Cornea
room. Irrigation should continue until the pH and External Disease. Vol. 2. St. Louis: Mosby; 1997:1437–1442.
of the eye normalizes. 14. Pfister RR, Pfister DA. Alkali-injuries of the eye. In: Krachmer
7. Small well-approximated conjunctival lacera- JH, Mannis MJ, Holland EJ, eds. Cornea: Fundamentals of
tions often heal without suturing. Cornea and External Disease. Vol. 2. St. Louis: Mosby;
1997:1443–1451.
15. Lubeck D, Greene JS. Corneal injuries. In: Mathews J, Zun LS,
REFERENCES
eds. Emergency Medicine Clinics of North America:
Ophthalmologic Emergencies and Ocular Trauma.
1. Fukuyama J, Hayasaka S, Yamada K, Setogawa T. Causes of Philadelphia: WB Saunders; 1988:82–86.
subconjunctival hemorrhage. Ophthalmologica 1990;200(2): 16. Roper-Hall MJ. Thermal and chemical burns. Trans
63–67. Ophthalmol Soc UK 1965;85:631–653.
2. Pitts JF, Jardine AG, Murray SB, Barker NH. Spontaneous 17. Brodovsky SC, McCarty CA, Snibson G, et al. Management of
subconjunctival haemorrhage: a sign of hypertension? alkali burns: an 11-year retrospective review. Ophthalmology
Br J Ophthalmol 1992;76(5):297–299. 2000;107(10):1829–1835.
3. Pearlman JA, Au Eong KG, Kuhn F, Pieramici DJ. Airbags and 18. Perry HD, Hodes LW, Seedor JA, Donnenfeld ED, McNamara
eye injuries: epidemiology, spectrum of injury, and analysis TF, Golub LM. Effect of doxycycline hyclate on corneal
of risk factors. Surv Ophthalmol 2001;46(3):234–242. epithelial wound healing in the rabbit alkali-burn model:
4. Kenyon KR. Recurrent corneal erosion: pathogenesis and preliminary observations. Cornea 1993;12(5):379–382.
therapy. Int Ophthalmol Clin 1979;19:169–195.
66
6
Closed globe injuries:
anterior chamber
James T. Banta, Colleen M. Cebulla, Carolyn D. Quinn
INTRODUCTION (with the larger pupil typically on the injured

side). The swinging flashlight test is used to rule
Contusive injuries to the anterior chamber are out a relative afferent pupillary defect. Intra-
exceedingly common. Although most are minor ocular pressure following a contusive injury can
and self-limited, permanent vision loss can result be elevated (due to mechanical blockage of the
if appropriate measures to detect severe injuries trabecular meshwork by hyphema or inflam-
are not initiated. The focus of this chapter will matory cells) or decreased (due to diminished
be to review the major traumatic injuries in- aqueous production associated with traumatic
volving the anterior chamber with a particular iritis).
emphasis on examination, stabilization, and Slit lamp examination is utilized to carefully
treatment. ascertain the status of anterior chamber struc-
tures. The conjunctiva is examined for the
EVALUATION presence of hemorrhage, lacerations, or foreign
bodies. The cornea is inspected for lamellar lac-
The assessment of an acute ocular injury begins erations, epithelial abrasions, or foreign bodies.
after other life-threatening injuries have been Increased magnification and a small, thin beam
appropriately ruled out. Once this has been are used to evaluate the anterior chamber for the
accomplished, a thorough history concerning the presence of cells and proteinaceous debris (flare).
mechanism of injury is of paramount impor- Circulating red blood cells are indicative of a
tance. Most injuries are due to projectile objects microhyphema, while white blood cells are seen
whether from assault, work, or play. The type of with traumatic iritis. The iris is carefully
object, the presence of sharp edges, and the inspected at the pupillary margin for iris sphinc-
speed the object was traveling should be specifi- ter tears. Typically a focal irregularity of the
cally recorded. pupil is present. Transillumination of the iris
If a possible open globe injury is suspected, a may reveal an iridodialysis or cyclodialysis. The
screening slit lamp examination should be per- remainder of the slit lamp and dilated fundus
formed prior to further testing. A complete examination should be carried out as outlined in
ophthalmic examination is then performed if the Chapter 3.
globe is intact. Visual acuity should be taken
with corrective spectacles if available. Pinhole PATHOPHYSIOLOGY
acuity may be used if spectacle correction is
unavailable. The use of a near card is sometimes Contusive injuries of the anterior segment (and
necessary in the emergency setting. Pupillary anterior portion of the posterior segment) share
examination is critical. Contusive ocular injuries a common mechanistic pathway. Force from a
frequently lead to traumatic mydriasis or iris blunt object typically indents the cornea sud-
sphincter tears which can lead to anisocoria denly and rapidly leading to rapid equatorial
67
Ocular trauma
dilator muscles), iris nerves, and ciliary body. 3,4

Interestingly, severe closed globe injuries fi rst
result in a transient miosis, followed by a long-
lasting partial mydriasis with poor pupillary
reaction.1,4 The ciliary body often develops
painful spasms and paralysis of accommodation
concurrently. Histopathologically, the ciliary
body contains a chronic inflammatory cell
infi ltrate, scarring, and atrophy, a likely ex-
planation for the occasional permanence of
inadequate accommodation following contusive
eye trauma.1
Diagnosis and treatment

Figure 6.1 Contusive injury of the globe leads to
The diagnosis of traumatic mydriasis is primarily
deformation of the cornea and subsequent equatorial
expansion of the globe. Aqueous is simultaneously based on slit lamp examination. If traumatic
forced into the periphery of the anterior chamber. mydriasis is the only lesion present, a large round
(Adapted with permission from Berke SJ. Post-traumatic pupil will be identified, whereas if iris sphincter
glaucoma. In: Yanoff M, Duker JS, eds. Ophthalmology, tears are present there may be a ‘D’-shaped
2nd edn. Philadelphia: Mosby; 2004:1518–1521.) margin, shallow indentations, or tears extending
the length of the iris.1 Multiple defects may be
expansion and forceful movement of aqueous present.
into the anterior chamber periphery (Figure Patients with ciliary spasm typically complain
6.1). The classic description of the seven areas of of dull, aching pain and photophobia. Cyclople-
traumatic ocular tears is illustrated in Figure gics paralyze the ciliary muscle, thereby prevent-
6.2. ing spasm and relieving pain. Treatment is
typically not needed outside the acute phase.
TRAUMATIC MYDRIASIS AND SPASM The prognosis of traumatic mydriasis and
OF ACCOMMODATION accommodative paralysis is generally good. While
the problems with pupillary dilation and accom-
Introduction modation are often transient, a small but signifi-
Traumatic mydriasis and spasm of accommoda- cant percentage of patients will experience
tion are frequent complications of ocular trauma.1 lasting dilation and mild visual effects from
Symptoms include eye pain, tearing, photo- accommodative paralysis.1,4 In an analysis by
phobia, discomfort when reading, and ocular Tönjum, 14 of 35 eyes with traumatic mydriasis
fatigue.1,2 The pupil is characteristically mid- and angle recession recovered a normal pupil size
dilated and poorly reactive to light with no rela- by 4 months after injury.4 In another series, only
tive afferent pupillary defect (Figure 6.3). 3 4 of 212 eyes with traumatic mydriasis were
permanently affected.5
Pathophysiology Photophobia and blurred vision are frequently
The force generated during contusive trauma encountered when traumatic mydriasis does not
results in injury to the iris (both sphincter and resolve spontaneously and the pupil remains
68
Closed globe injuries: anterior chamber
3. Anterior ciliary body

– angle recession
2. Iris base 4. Ciliary body to scleral spur

– iridodialysis – cyclodialysis cleft
2
4
1. Iris sphincter 5. Trabecular meshwork
– radial tears – TM tears
6
5
7. Retina to ora serrata 6. Zonules

– retinal detachment and dialysis – lens subluxation and dislocation
Figure 6.2 The seven areas of traumatic ocular tears with resultant findings. (Adapted with permission from
Campbell DG. Traumatic glaucoma. In: Shingleton BJ, Hersh PS, Kenyon KR, eds. Eye Trauma. St. Louis: CV Mosby;
1991:117–125.)
enlarged. Symptomatology correlates with the

size of the pupil. Pilocarpine is sometimes given
to reverse mydriasis, but induced myopia in
young patients limits its usefulness. If pilocar-
pine use is attempted, a very dilute formulation
(0.25% or less) should initially be used in an
Figure 6.3 Traumatic mydriasis is seen in the right eye attempt to diminish unwanted side-effects. If
following an industrial accident. A painted contact lens
unsuccessful, the concentration can be escalated
was successfully used to limit debilitating glare induced
until symptoms diminish or side-effects become
by the enlarged pupil.
prohibitive. Side-effects of pilocarpine include
induced myopia, brow ache, ciliary spasm,
69
Ocular trauma
conjunctival injection, and reduced visual acuity Diagnosis and treatment

in dim illumination, particularly if lens opacities Photophobia, pain, and blurred vision are the
are present. Thymoxamine, an alpha antagonist, symptoms most frequently elicited. Although
has shown some effectiveness in small clinical symptoms can arise rapidly following severe
trials, but is seldom used clinically. Tinted injuries, the presentation is often delayed 3–4
contact lenses are an excellent option to improve days following a mild contusive injury.
functionality and cosmesis. Hand-painted as As mentioned above, the IOP can be quite
well as dyed lenses are commercially available variable although relative hypotony compared to
and assist in decreasing glare and photophobia. the uninvolved eye is most frequently encoun-
Finally, surgical repair of the iris can be consid- tered. Diagnosis of traumatic iritis requires
ered in conjunction with other procedures such visualization of anterior chamber cells and flare.
as cataract extraction. These fi ndings are best seen under high magni-
fication with a short, narrow slit beam placed
TRAUMATIC IRITIS tangentially at maximum intensity. Prominent
perilimbal injection is often seen and is referred
Introduction to as a ciliary flush.
Traumatic iritis is one of the most frequent fi nd- The treatment of choice for traumatic iritis is
ings after contusive ocular trauma. Symptoms cycloplegia (isoptohyoscine or atropine 1% two
are similar to other forms of iritis and include to four times daily) alone or in combination with
pain, photophobia, and mildly decreased vision. a steroid drop (prednisolone acetate 1% four
The intraocular pressure (IOP) is often lower in times daily). Treatment is typically necessary for
the injured eye due to ciliary body dysfunction, only a short time (1–2 weeks), although a more
although elevated IOP can occur.6 The classic persistent and exuberant cellular reaction has
slit lamp fi nding is anterior chamber cells and been described.6
flare. Traumatic iritis is often seen in conjunc-
tion with traumatic mydriasis and spasm of IRIS SPHINCTER TEARS
accommodation. AND IRIDODIALYSIS
Pathophysiology Introduction
Contusive ocular trauma causes an initial vaso- Iris sphincter tears and iridodialyses are com-
spasm of the anterior uveal vessels, followed by monly seen after contusive trauma to the eye.
hyperpermeability. 3 This permeability allows a Patients with iris sphincter tears or iridodialyses
delayed leakage of protein and fibrin into the may complain of changes to the shape of the
anterior chamber. A transient, scant release of pupil, monocular diplopia (if the tear permits
white blood cells typically occurs in this period. light to travel to the retina outside the visual
Rarely, a more severe uveitis may develop, even axis), glare, decreased vision, and sensitivity to
creating an endophthalmitis-like presentation. light.
Histopathologically, chronic inflammatory cells
are demonstrated infi ltrating the ciliary body.1 Pathophysiology
The ciliary body inflammation typically leads to Iridodialysis is the shearing of the iris from the
hypoproduction of aqueous fluid and subsequent ciliary body at the iris root. The iris is thinner
lowering of intraocular pressure. at this point, and more susceptible to injury.
70
Kumar et al experimentally examined the mech- the suprachoroidal space, is present in the gonio-
anism of this injury, exposing enucleated porcine scopic view of cyclodialysis. In iridodialysis, the
eyes to contusive trauma at either 90 or 30 iris is separated at its root (Figure 6.6).
degrees to the iris plane.7 The 30-degree approach No treatment is necessary for iris sphincter
resulted in a more severe iridodialysis, indicating tears. Any associated hyphema should be
the importance of side protection on safety managed as outlined in the hyphema section.
glasses. Iridodialysis only rarely requires treatment. The
indications for surgical repair include:
Diagnosis in a patient with an appropriate history
of ocular trauma is primarily by slit lamp exami-
nation. Iris sphincter tears can present as single
or multiple point-like lesions at the pupil margin,
shallow indentations, or tears extending the
length of the iris.1 The pupil often takes on a
‘D’-shaped configuration (Figure 6.4). Small
hemorrhages on the iris, microhyphema, or
hyphema may be present. Iridodialysis may
appear as a small, crescent-shaped black area in
the anterior chamber periphery (Figure 6.5).
Large iridodialyses can lead to severe disruption
Figure 6.5 An inferior iridodialysis is seen in a patient
of normal iris architecture.8 Gonioscopy is
who was struck with a thrown rock as a child. Note the
necessary to differentiate iridodialysis from the bunching of the iris at the superior margin of the
more serious cyclodialysis.9,10 A gap between iridodialysis and the subsequent blunting of the
the sclera and the ciliary body, with widening of pupillary margin.
Figure 6.6 Gonioscopy photo of the same patient

pictured in Figure 6.5 showing the disinsertion of the
Figure 6.4 D-shaped pupil deformity is seen following iris root leading to prominent visualization of the ciliary
a severe contusive injury. processes.
71
Ocular trauma
1. refractory monocular diplopia of this technique (McCannel suture technique)

2. debilitating glare11 utilize a double-armed suture. Both arms of the
3. expulsive iridodialysis (a rare condition in trau- suture pass through the damaged iris several
matized eyes with a history of ocular surgery)12 millimeters apart and exit under a scleral flap
4. repair in conjunction with other planned posterior to the limbus. The sutures are secured
anterior segment surgery under the flap creating a mattress suture.8,13,14
5. cosmesis Closed chamber surgical techniques using
6. subtotal iridodialysis associated with needles that hold a suture have also been used
8
glaucoma. successfully to treat iridodialysis without creat-
Several surgical techniques have been described ing an incision in the anterior chamber.15–17 Iri-
to treat iridodialysis. Removal of iris tissue may dodialysis repair has been successfully combined
be necessary if necrosis ensues, but repositioning with other anterior chamber surgeries such as
is always preferred if possible. Original surgical trabeculectomy, pars plana vitrectomy, and cata-
techniques utilized a 10-0 polypropylene suture ract surgery.18–20 Complications are uncommon,
on a 17 mm straight needle inserted 180 degrees but suture erosion has been described and is of
from the center of the iridodialysis and passed particular concern in children and young adults
through the damaged iris before being secured because of softer sclera and a longer duration the
to the sclera under a scleral flap. Popular variants sutures will remain in place.10
CASE EXAMPLES
Case report: iridodialysis (Figure 6.7)

A 16-year-old male reports glare, monocular diplopia lens implantation. Using a McCannel suture tech-
and decreased vision in the left eye 4 months after nique, the iris was reapproximated nasally and the
suffering a paintball injury. He initially had a small sutures were buried under a partial-thickness scleral
hyphema which was treated uneventfully. Initial flap (C). Postoperatively, the patient recovered vision
visual acuity was 20/40. Examination of the left eye to 20/20 with complete resolution of the monocular
revealed a large nasal iridodialysis and an anterior diplopia and glare. Anatomically, the iris was reap-
subcapsular cataract (A). The patient subsequently proximated with minimal distortion of the pupil
underwent phacoemulsification (B) with intraocular (D).
A B
Included
on DVD
72
Case report: iridodialysis (cont’d)
C D
HYPHEMA
Introduction
Hyphema is a condition in which blood accu-
mulates in the anterior chamber (Figure 6.8).
Approximately two-thirds of traumatic hyphe-
mas are seen with closed globe injuries and
one-third in open globe injuries. The mean
annual incidence of hyphema is 17 per 100 000,
with a peak age between 10 and 20 years of
age.21
Presenting symptoms include pain, photopho-
Figure 6.8 A typical layered hyphema following
bia, and decreased vision. If a microhyphema is contusive ocular injury.
present (red blood cells suspended in the ante-
rior chamber with no layering of blood), the equatorial globe expansion. Depending on the
patient may have a presentation very similar to force exerted and the extent of vascular damage,
traumatic iritis. varying amounts of blood enter the anterior
Concomitant injury of the anterior chamber is chamber.22 At the time of injury, the IOP can be
exceedingly common when a hyphema is present. quite variable and does not necessarily correlate
Iris sphincter tears, iridodialyses, cyclodialyses, with the amount of bleeding. The pressure can be
and lenticular abnormalities (e.g. cataract, dislo- elevated as a result of obstruction of the trabe-
cation) frequently coexist. cular meshwork by clot, circulating red blood
cells, and/or inflammatory debris. Rarely, a collar-
Pathophysiology button-shaped clot can cause pupillary block
During a contusive injury to the eye, the ante- resulting in an elevated pressure.23 Intraocular
rior–posterior force ultimately causes disruption pressure can also be low initially due to ciliary
of the ciliary body, iris stroma, and the major body inflammation and diminished aqueous
arterial circle and its branches by simultaneous production.
73
Ocular trauma

Slit lamp examination typically reveals red blood
cells and proteinaceous debris suspended in the
anterior chamber and an inferiorly layered clot
in the anterior chamber. In an ‘8 ball’ hyphema,
the entire anterior chamber is fi lled with blood
and intraocular structures cannot be identified.
The IOP can be quite variable at the time of
initial examination; however, if the pressure is
low and the posterior chamber cannot be visual-
ized, an eyewall violation must be suspected. At
the time of initial examination the visual acuity,
the IOP, and the amount of blood in the anterior Figure 6.9 Corneal blood staining clears peripherally to
centrally over many months.
chamber should be documented. If the patient is
African-American and/or has a positive family
history of a sickling hemoglobinopathy, an appro-
priate laboratory evaluation should be completed years, hyphema patients have routinely been
at the fi rst visit. Aspirin, anti-platelet therapy, followed as outpatients. Multiple studies have not
and non-steroidal anti-inflammatories should be demonstrated a statistically significant difference
avoided in patients with hyphemas. between the two treatment strategies.23–26 Shiuey
The ideal treatment of a hyphema, despite cen- and Lucarelli compared 154 patients managed as
turies of experience, is still somewhat controver- outpatients with 119 historic controls (people
sial. The goal of treatment is threefold: managed as inpatients) and found the rebleed
1. to improve patient comfort rate was 5% and 4.5% respectively.27
2. to prevent rebleeding Currently, the vast majority of patients with
3. to monitor for complications (elevated IOP, hyphemas are treated as outpatients. Inpatient
corneal blood staining). management should be considered in the follow-
Rebleeding typically occurs 3–5 days after the ing situations:
initial injury and is often much larger than the 1. severe, recalcitrant IOP elevation
initial bleed. The percentage of patients who 2. follow-up cannot be assured
rebleed after the initial injury varies from 0% to 3. hyphema in the setting of a sickling
38%. Corneal blood staining is an infrequent hemoglobinopathy
condition that can also occur following hyphema. 4. very young children with hyphemas.
Elevated IOP and endothelial toxicity can lead Cycloplegics, such as atropine 1%, are used to
to entry of blood breakdown products into the prevent posterior synechiae (adhesions between
corneal stroma (Figure 6.9). Careful examina- the iris and lens) and to decrease photophobia,
tion for the presence of corneal blood staining accommodative spasm, and pain. To date, no
needs to be performed at each follow-up visit, studies have shown that treatment with cyclo-
particularly in the setting of a rebleed or pro- plegics affects visual outcome or incidence of
longed elevation of IOP. rebleeding.
Classic teaching dictated strict bed rest and Corticosteroids are a mainstay of treatment for
hospitalization following hyphema, but in recent hyphema. It is postulated that inhibiting fibrino-
74
lysis with corticosteroids may decrease the inci- 2. Cycloplegia is maintained with scopolamine
dence of rebleeding. In a retrospective report of or atropine.
463 eyes, Ng et al. reported a decrease in rebleed- 3. An eye shield is worn full-time.
ing from 12% to 5% when topical steroids were 4. Instructions are given to maintain bed rest
utilized.28 Systemic steroids have also been with minimal ambulation only when neces-
reported to reduce the rate of secondary bleeding sary (‘bathroom privileges’).
in multiple studies.21,23,29–31 No prospective 5. Patients are encouraged to remain upright or
studies have established the optimal dose or fre- keep the head of their bed angled at more
quency of topical or systemic steroids. than 45 degrees.
Aminocaproic acid is an anti-fibrinolytic agent 6. Warning signs of rebleeding and elevated
that has been utilized to reduce the incidence of IOP are fully discussed with the patient
secondary hemorrhage following traumatic (increased pain and decreased vision in
hyphema. Systemic aminocaproic acid has been particular).
shown to reduce the rate of secondary hemor- 7. The importance of daily follow-up is
rhage in a significant fashion. 32 The widespread discussed.
acceptance of this therapeutic modality has been Medical therapy for elevated intraocular pres-
hampered by frequent systemic side-effects, sure adds another level of complexity to the
expense, and difficulty obtaining the medicine. treatment strategy. It is vital to ascertain the
More recently, a topical gel formulation of possible status of sickling hemoglobinopathies,
aminocaproic acid has been studied. It currently since this has a direct impact on the types of
is not Food and Drug Administration (FDA) medication that can be utilized. Carbonic
approved for this or any medical use. In Phase anhydrase inhibitors (oral acetazolamide and
II and III FDA studies, the rate of rebleeding methazolamide, topical dorzolamide and apra-
was decreased similar to that seen with sys- clonidine) should be avoided in patients with
temic therapy. 33,34 It is possible that this will sickling hemoglobinopathies as they lower
eventually become a viable therapeutic option oxygen tension in the anterior chamber and
if and when further investigation is completed. lead to rapid sickling of red blood cells within
However, a question remains as to whether the anterior chamber. Sickled red blood cells
aminocaproic acid is superior to topical steroids, more readily block the trabecular meshwork
an alternative that has been routinely used for and can lead to rapid elevations in IOP. Fur-
many years and is readily available. The only thermore, patients with sickle cell anemia are
study comparing the two found no difference in more prone to ischemic events of the optic
the rate of secondary hemorrhage.29 nerve, even with mild rises in IOP, and must be
The authors prefer the following regimen for monitored more closely. In patients without
outpatient management of hyphema without sickle cell, all classes of IOP-lowering medica-
intraocular pressure elevation: tions can be safely used except for pilocarpine.
1. Topical prednisolone acetate 1% used four Pilocarpine should be avoided as it may incite
times daily to hourly depending on the further inflammation, increase the risk for pos-
extent of hyphema and degree of inflam- terior synechiae, and limit the examination of
mation. In patients who are unable to ad- the retina. Beta-blockers, alpha agonists, and
minister drops, systemic steroids may be carbonic anhydrase inhibitors can all be effective
used. in controlling IOP in the setting of hyphema.
75
Ocular trauma
Table 6.1 Commonly used agents for acute elevations of intraocular pressure
Drug Dosage Common Onset/duration Comments

side-effects of action
Acetazolamide 500–1000 mg Fatigue, taste Tablets: 1 hour/8–12 Initial 500 mg given acutely
(tablets or in divided disturbances hours as two 250 mg tablets;
sustained- doses Sustained-release sustained-release capsules
release capsules) capsules: 2 hours/ preferable for extended
18–24 hours use owing to longer
half-life; avoid if patient
has sulfonamide allergy
Mannitol 1.5–2 g/kg Headache, 30 minutes/4–6 hours I.V. preparation given

as a 20% I.V. nausea slowly over 30–45 minutes;
solution contraindicated in patients
with congestive heart
failure, renal failure, or
pulmonary edema; excellent
choice if patient has nausea
and vomiting
Isosorbide 1.5 g/kg as Headache, 1 hour/4–6 hours Served over ice and sipped
an oral nausea slowly over 30–60 minutes;
solution preferable over glycerin for
diabetic patients
Glycerin 1–2 g/kg Headache, 1 hour/5 hours Served over ice and sipped
as an oral nausea slowly over 30–60 minutes;
solution can cause severe serum
glucose elevations in diabetic
patients
Although prostaglandin analogues can theore- in diabetics as it can lead to precipitously ele-
tically promote or enhance inflammation, the vated blood sugar. All hyperosmotic agents
authors routinely use them in the setting of can exacerbate congestive heart failure, pulmo-
elevated intraocular pressure associated with nary edema, or hypovolemia and should be
hyphema and have yet to recognize a detrimental used with great caution and under appropriate
effect. observation. Intravenous mannitol can rapidly
In the acute setting of severely elevated IOP, reduce the intraocular pressure and is a good
oral carbonic anhydrase inhibitors and oral or alternative for the patient with severe nausea and
intravenous hyperosmotic agents are effective in vomiting.
quickly reducing the IOP (Table 6.1). Oral Topical and oral medications can be used for
hyperosmotic agents like isosorbide and glycerin outpatient IOP control. Our typical regimen for
are often used initially if not medically contra- hyphema-related IOP elevation includes some
indicated. Glycerin should be used with caution combination of the following:
76
1. combination timolol/dorzolamide drops twice Surgical techniques to lower intraocular pres-

daily sure following hyphema include anterior chamber
2. brimonidine drops twice daily (AC) washout with or without trabeculec-
3. oral acetazolamide tomy. 35,36 It is vital to minimize the amount of
4. prostaglandin analogue once daily. manipulation during surgery. AC washout uti-
Surgical intervention is sometimes necessary lizes an entry and an exit paracentesis placed
when IOP is not controlled adequately with 180 degrees away from one another. As balanced
medical therapy or if corneal blood staining salt solution is gently irrigated into the eye, the
occurs. Prolonged elevated IOP can cause pro- opposite paracentesis is gaped to allow gentle
gressive optic nerve injury leading to decreased egress of the blood clot. The goal of AC washout
vision and visual field defects. An ischemic is to debulk the organized hyphema present in
optic neuropathy can be induced by a severely the anterior chamber, thereby removing a portion
elevated IOP or even a moderately elevated of the mechanical blockage of the trabecular
IOP in patients with sickle cell anemia. Corneal meshwork that is partially responsible for ele-
blood staining can severely limit visual acuity vated IOP. Excessive manipulation and vigorous
and can cause amblyopia in children. The timing irrigation should be avoided. The addition of a
of surgical intervention depends greatly on the trabeculectomy to AC washout allows continued
extent and duration of IOP elevation and the egress of blood and aqueous, both lowering IOP
presence of corneal blood staining. Criteria and allowing more blood to exit the eye while
for surgical intervention developed by Read24 relieving pupillary block (if present). 37 The tra-
include: beculectomy often fails after a short period of
1. microscopic corneal blood staining time, a result that is expected and in most cases
2. total hyphema with intraocular pressures of desirable.
50 mmHg or more for 5 days (to prevent optic The authors often utilize small-gauge biman-
nerve damage) ual vitrectomy through limbal corneal incisions.
3. hyphema that is initially total and does not The separation of irrigation and vacuum while
resolve below 50% at 6 days with intraocular maintaining a relatively closed environment
pressures of 25 mmHg or more (to prevent allows for a gentle, controlled removal of the
corneal blood staining) hyphema. It is vital to maintain the least amount
4. hyphema that remains unresolved for 9 days of flow possible to remove the hyphema and
(to prevent peripheral anterior synechiae). avoid excessive manipulation within the anterior
When sickling hemoglobinopathies are present, chamber. The crystalline lens, iris, and corneal
criteria for surgical intervention are more endothelium should be given a wide berth to
stringent: avoid iatrogenic injury. Whatever method is
1. repeated IOP measurements over 30 mmHg used, the goal is only to debulk the organized
2. mean IOP > 24 mmHg in the fi rst 24 hours hyphema. Overzealous attempts to completely
following injury. clear the anterior chamber can cause rebleeding
These guidelines are tailored to the clinical situ- or damage to intraocular structures.
ation and are not considered hard and fast rules.
77
Ocular trauma
CASE EXAMPLES
Case report: hyphema (Figure 6.10)

A 17-year-old male accidentally poked himself in the The decision was made to proceed with removal of
right eye with the blunt end of a writing pen. He the anterior chamber clot. Bimanual vitrectomy
noted immediate decreased vision and pain. He pre- instrumentation was introduced through two limbal
sented to the emergency room with a visual acuity incisions and the clot was removed successfully (B).
of light perception in the involved eye and an intra- The iris and lens were given a wide berth throughout
ocular pressure of 10. A 1.5 mm hyphema was noted the procedure. The pressure decreased from 35 on
in the anterior chamber. The patient was started on the first postoperative day to 14 on the third post-
topical steroids and cycloplegia and instructed to operative day. The anterior chamber remained free
return the next day. The patient returned the follow- of blood. Once the clot had been removed, an iris
ing day complaining of increased pain. A complete sphincter tear was now visible superiorly leading
hyphema was now present although intraocular to a typical D-shaped deformity of the pupil.
pressure remained normal. Over the course of a week, Importantly, it was apparent the anterior lens capsule
although the hyphema began to contract into a had been successfully avoided as retroillumination
central clot (A), intraocular pressure continued to revealed a clear lens (C). The patient recovered vision
increase despite aggressive medical therapy. Six days of 20/25.
after initial presentation, intraocular pressure was 51.
A B
78
Case report: hyphema (cont’d)

All cases are not equally successful. Despite prompt (F) were performed. Although the anterior chamber
and appropriate care, poor outcomes are frequently washout was initially successful, reaccumulation of
encountered, often related to concomitant injuries. the anterior chamber blood was noted in the follow-
A 15-year-old male was punched in the right eye. ing days. The intraocular pressure was better con-
Initially he complained of pain, but his vision was trolled following surgery. The situation became more
only mildly blurred. Four days following the injury, complicated when a follow-up ultrasound revealed
he experienced sudden onset of severe pain and a retinal detachment. Pars plana vitrectomy and
decreased vision. Initial evaluation of the right eye lensectomy were performed to repair a giant retinal
revealed a vision of light perception and an intraocu- tear with an associated fibrotic retinal detachment.
lar pressure of 50. Slit lamp examination revealed a Silicone oil tamponade was utilized. In the following
total hyphema (D). The patient was started on days, the hyphema reaccumulated once again and
aggressive medical treatment to control the intra- pressures were again elevated, likely due to anterior
ocular pressure. He initially received isosorbide and movement of silicone oil. Corneal blood staining was
later intravenous mannitol. Despite maximum soon evident (G). Despite slow clearing of the corneal
medical therapy, pressure remained in the 30s. A blood staining, vision never improved beyond light
decision was made to intervene surgically. An perception.
anterior chamber washout (E) and trabeculectomy
D E
Included
on DVD
F G
79
Ocular trauma
Complications and outcomes of whom were African-American and sickle cell

As illustrated in the case reports, the visual trait positive. The rate of rebleeding in Cauca-
prognosis for patients with hyphema is quite sian and non-sickle cell trait African-American
variable and depends on intraocular pressure, children was 0%. Overall, nine of 14 patients
rebleeding, the amount of blood at presentation, (64%) who tested positive for sickle cell trait had
and the presence of concomitant injury. rebleeding.41
Rates of corneal blood staining vary depending Patients with sickling hemoglobinopathies are
on the size of the initial hyphema and the extent more susceptible to vascular occlusive events at
and duration of elevated intraocular pressures. lower pressures than normal individuals. Central
However, there have been multiple reports of retinal artery occlusions in sickle cell patients
patients with normal IOP and a small hyphema with pressures between 30 and 39 mmHg have
who develop visually significant corneal blood been reported.41,42 Dehydration can lead to
staining.26,38 It is postulated that the combina- hyperviscosity and an increased risk of vascular
tion of endothelial cell dysfunction and the toxic occlusion. For this reason, systemic hyperos-
effect of the blood breakdown products allows motic agents and diuretics should be used with
the penetration of hemoglobin and hemoglobin great caution or avoided entirely. As described
breakdown products into the posterior stroma. 39,40 above, carbonic anhydrase inhibitors should
Initially the deep stroma will have a yellowish always be avoided because they promote anterior
discoloration and pigment granules can be seen chamber sickling due to induced acidosis.
in the posterior one third of the cornea. Close Other complications of hyphema include
examination of the posterior corneal is critical in peripheral anterior synechiae, optic atrophy (due
all patients with hyphemas. Corneal blood stain- to contusion of the optic nerve, elevated intra-
ing initially clears in the periphery of the cornea ocular pressure, or vascular occlusion), accom-
and can take months to years to completely clear modative impairment, cataract formation, and
centrally. 38 Corneal blood staining can have angle recession.24,26 Visual acuity outcomes for
potentially devastating results in children due to hyphema can be quite variable. Approximately
deprivation amblyopia, and penetrating kerato- 75% of patients will achieve a visual acuity of
plasty may be necessary to prevent severe 20/50 or better.43 In a recent prospective study,
amblyopia. Rocha et al. reported a series of 35 children of
The prevalence of sickle cell trait in the African- whom 75% achieved a visual acuity of 20/25
American population is approximately 10%.41 or better.44 Poor visual acuity outcomes were
Patients with sickle cell trait and sickle cell due to retinal detachment, lens subluxation,
disease are at risk for developing severe IOP commotio retinae, and vitreous hemorrhage.
spikes, as sickled red blood cells in the anterior Although nearly half of these patients had ele-
chamber readily obstruct the trabecular mesh- vated IOP (>24 mmHg), all were controlled with
work. In all African-American patients a careful medical therapy.
history should be taken and a sickle cell prepara-
tion should be ordered, even if family history is ANGLE RECESSION
negative. In addition to the rapid IOP rises, sickle
cell patients are also at a higher risk for rebleed- Introduction
ing. In a published series of 99 children with Angle recession is an uncommon, yet underdiag-
hyphema, nine patients (9%) had rebleeding, all nosed entity. Any severe contusive trauma,
80
particularly if severe enough to cause hyphema,

is highly correlated with angle recession.
Although commonly seen after eye trauma, only
a small percentage of patients will go on to
develop glaucoma. The silent nature of the con-
dition underlies the importance of longitudinal
follow-up after severe contusive ocular trauma.
Pathophysiology
As seen in Figure 6.1, contusive ocular injury
leads to a decrease in anterior–posterior length
and rapid equatorial expansion. Aqueous forced
into the periphery of the anterior chamber angle
Figure 6.11 Gonioscopic view of angle recession with a
can create a split in the ciliary body. The longi- broad yet irregular band of visible ciliary body. Note
tudinal muscle of the ciliary body remains the irregular, undulating contour of the iris root.
attached to the scleral spur while the circular
muscle of the ciliary body and the iris root are
forcefully separated.45 This leads to a deepening pigment deposition, tears in the iris sphincter,
and widening of the anterior chamber angle. iridodialysis, iridodonesis, phacodonesis, and
Small branches of the anterior ciliary artery are focal cataract formation are clues to prior signifi-
often injured during this process, which explains cant ocular injury.
the frequent coexistence of hyphema and angle Subtle changes include disruption of the iris
recession.46 processes from their insertion into the scleral
The development of glaucoma associated with spur and ciliary body leaving the ciliary body
angle recession is not fully understood. Scarring more exposed.51 In more severe injuries, the
of the trabecular meshwork, loss of intertrabecu- degree of angle recession may be larger and man-
lar spaces, and scarring of Schlemm’s canal ifest as a widened ciliary body band and a more
results in decreased aqueous outflow and subse- prominent scleral spur (Figure 6.11). Often it is
quent elevations in IOP.47–51 The greater the necessary to compare the width and color of the
portion of angle involved, the greater the subse- ciliary body band to the fellow eye if the entire
quent risk of glaucoma. Glaucoma rarely devel- angle is involved. It is important to assess the
ops if less than 180 degrees of angle is extent of the angle recession. The extent of angle
involved. involvement is directly correlated to the future
development of glaucoma.47
Diagnosis and treatment After establishing the extent of the angle
Gonioscopy is the mainstay of diagnosis in angle involved, it is critical to emphasize to the patient
recession. It is avoided during the acute phase of the need for lifelong follow-up. Careful docu-
Included
ocular injury if a hyphema is present. The angle mentation of the IOP and optic nerve should be
on DVD
appearance can be quite variable after a contu- completed. Initially, the IOP can be managed
sive injury and it is best to compare the angles medically. Miotics should be avoided because
of both eyes using a Zeiss or Goldman lens. Signs they are ineffective and can rarely cause an ele-
of previous trauma including corneal scars, vated IOP due to a decrease in uveoscleral
81
Ocular trauma
outflow. All other classes of glaucoma medica- Pathophysiology

tions may be effective. Laser trabeculoplasty is Rapid equatorial expansion of the eye during
usually ineffective in cases of traumatic glau- contusive injury can cause disinsertion of the
coma.52,53 Ultimately, many patients with angle ciliary body from the scleral spur. Historically,
recession glaucoma are inadequately controlled communication between the anterior chamber
and require surgical intervention. and suprachoroidal space following cyclodialysis
was confi rmed surgically when fluorescein was
Complications and outcomes injected into the anterior chamber, and fluores-
Approximately 6–8% of patients with angle cein staining of the fluid drained externally from
recession will ultimately develop glaucoma.47,51 the suprachoroidal space was noted. The free
It is possible that patients in this group also have passage of aqueous into the suprachoroidal
a predisposition to develop glaucoma, given that space leads to hypotony as the potential space of
50% of patients with traumatic glaucoma will the suprachoroidal space has a much greater
develop primary open angle glaucoma in their volume than the anterior chamber. Ciliochoroi-
fellow eye.54 If the IOP is not adequately con- dal detachments often form and lead to further
trolled, progressive optic neuropathy can occur. dysfunction of the ciliary body, diminished
Prior to the use of anitmetabolites such as 5- aqueous production, and further hypotony.
fluorouracil and mitomycin-C, trabeculectomy These two factors in concert with inflammation
success rates were disappointing with rates as from the inciting trauma often lead to profound
low as 6–8% 5 years postoperatively.55 Manners hypotony,57,58 the hallmark of a cyclodialysis
et al recently reported a series of 41 patients who cleft.
underwent trabeculectomy with mitomycin C
for traumatic glaucoma with an improved success Diagnosis and treatment
rate of 85% at 1 year and 66% at 3 years.56 Other The diagnosis of cyclodialysis depends primarily
surgical options include the use of drainage on tonometry, slit lamp examination, gonios-
device implants. Ultimately the visual acuity copy, and dilated fundus exam.59 Blurred vision
outcome depends on the presence of coexisting with a hyperopic shift may be present due to
ocular injuries and adequate IOP control. anterior displacement of the lens–iris diaphragm
and overall shortening of the eye. Hypotony,
CYCLODIALYSIS often profound, is the classic fi nding. Anterior
chamber signs include corneal edema, shallow-
Introduction ing of the anterior chamber, mydriasis, and a
Traumatic cyclodialysis is an uncommon condi- peaked pupil near the cyclodialysis site. If hypo-
tion and can sometimes be difficult to diagnose. tony is persistent, optic disc edema, retinal vessel
A cyclodialysis cleft forms when a portion of the tortuosity, and retinal and choroidal folds are
ciliary body is disinserted from the sclera, allow- often seen.59,60 Many cyclodialyses can be visual-
ing free passage of aqueous into the suprachoroi- ized with gonioscopy and appear as a gap between
dal space. Eye pain, tenderness, and decreased the sclera and the ciliary body. Ultrasound bio-
vision are common presenting symptoms. Severe microscopy is a newer technique which offers
hypotony is the hallmark of the condition and promise in diagnosing occult cyclodialyses, espe-
can lead to corneal failure and eventually phthi- cially when the view is obscured by hemorrhage
sis bulbi if left untreated. or corneal edema.61,62 Cyclodialysis clefts become
82
increasingly difficult to visualize as time passes, ening the anterior chamber and exposing the
as peripheral anterior synechiae form and obscure cleft for laser therapy.59
the anterior chamber angle.50 Ultrasound can Although many cyclodialysis clefts respond to
facilitate diagnosis and localization in these more laser treatment, invasive surgical treatments are
difficult cases. recommended if argon laser therapy fails.59,64–67
Many treatments have been developed for The classic treatment of diathermy described
cyclodialysis.59 Observation or medical therapy by Maumenee and Stark remains a reasonable
with cycloplegics is initially attempted, but second-line therapy.63 Direct cyclopexy has been
further treatment is often required to defi ni- more recently advocated. In this technique, the
tively close the cleft. Atropine is used initially to ciliary body is sutured directly to the sclera in
maintain anatomic proximity of the ciliary body the area of the cleft by way of a partial- or full-
and scleral spur, thereby encouraging closure of thickness scleral flap. Indirect cyclopexy has also
the cleft. Corticosteroids are thought to delay been reported using a McCannel suture similar
closure of cyclodialysis clefts, and are generally to repair of iridodialysis, and this technique may
not recommended unless required for concomi- be effective for smaller clefts. Anterior scleral
tant injuries. buckle may be effective, especially if the cleft
The classic treatment of cyclodialysis for many area is very large.
years was pupillary dilation in conjunction with Other generally less invasive techniques have
diathermy applied to the cyclodialysis cleft, fol- also been reported to be successful in treat-
lowed by drainage of suprachoroidal effusions ing cyclodialysis including cryotherapy, YAG
through incisions in the sclera.63 Flattening the laser cyclophotocoagulation, and argon laser
communication with the suprachoroidal space endophotocoagulation.68–72
would often lead to reattachment of the ciliary
body and restoration of function. In an impor- Complications and outcomes
tant treatment advance, Joondeph was the fi rst Successful treatment of cyclodialysis results in
to use argon laser to successfully treat cyclodialy- closure of the cleft and an acute increase in IOP
sis.60 Argon laser applied to the cyclodialysis and eye pain.58,59 Patients should be instructed
cleft has now become the fi rst line of therapy if to contact their physician if they experience
medical management does not achieve success in severe eye pain. The rise in IOP is typically
the fi rst 4–6 weeks.58 Laser is applied to the delayed by 1–2 weeks when indirect treatments
ciliary body and scleral sides of the cleft. Recom- are used (e.g. argon laser) but can be very rapid
mended settings are: following direct cyclopexy. This ocular hyper-
1. duration of 0.1 second tensive period is typically transient and thought
2. 50–100 micron spot size to be due to delayed opening of aqueous drainage
3. 500–1500 mW power channels that collapse during prolonged hypoto-
4. approximately 100 applications. nous periods. Topical and oral aqueous suppres-
Atropine is continued after treatment. If the sants are used to manage these transient episodes.
initial treatment is unsuccessful, repeat treat- Pilocarpine can facilitate reopening of the cleft
ments often will close the cyclodialysis cleft. If and should be avoided.
the anterior chamber is relatively flat, obscuring The prognosis of cyclodialysis with treatment
the view of cyclodialysis clefts, viscoelastic injec- is surprisingly good.59 Although delayed closure
tion into the anterior chamber is helpful in deep- may reduce visual acuity, patients have been
83
Ocular trauma
reported to improve even after long periods of hypotony.72 Concomitant traumatic injuries of
hypotony, including one case of visual improve- the posterior segment are often responsible for
ment from 20/200 to 20/30 after 7 years of poor visual outcomes when they occur.
CASE EXAMPLES
Case report: cyclodialysis cleft (Figure 6.12)

A 26-year-old male was hammering a nail when the One week later, the patient presented to the emer-
nail became dislodged and struck him in the left eye. gency clinic again with complaints of pain in the left
He was placed on atropine and prednisolone acetate eye. Vision had improved to 20/70 and intraocular
by an ophthalmologist. A month later, he presented pressure was 34. Timolol and dorzolamide were
to our emergency clinic with complaints of declining applied and the intraocular pressure was quickly
vision in the left eye. Initial visual acuity was 20/200 normalized. Vision continued to slowly improve. At
in the left eye with an intraocular pressure of 6. Slit the final follow-up 18 days following the second
lamp examination revealed a subtle abnormality in round of argon laser photocoagulation, visual acuity
the contour of the temporal pupillary margin and a was 20/20 and intraocular pressure was normal.
suspicious area in the temporal anterior chamber Dilated fundus exam revealed vast improvement in
angle (A). Gonioscopy revealed a temporal cyclo- the optic nerve edema and vascular tortuosity,
dialysis cleft (B). Dilated fundus exam revealed although some retinal folds persisted (E). Before and
optic nerve edema, retinal vascular tortuosity, and after OCT evaluation shows marked improvement in
macular edema with retinal folds (C). A diagnosis of macular edema, subretinal fluid, and chorioretinal
hypotony maculopathy secondary to the cyclodialy- architecture (F). (From Goldman D, Moore J, Greulich
sis cleft was made. Argon laser photocoagulation K, Flynn HW Jr. Cyclodialysis and hypotony macu-
was applied to the bed of the cleft and prednisolone lopathy. Ophthalmic Surgery, Lasers & Imaging.
acetate was tapered quickly. Atropine was continued 37:438–9, 2006 with permission from SLACK
four times daily. Four days later, the situation was Incorporated.)
unchanged and further argon laser was applied (D).
A B
84
Case report: cyclodialysis cleft (cont’d)
C D
E F
SUMMARY 4. Large traumatic iridodialyses may lead to

chronic glare and diplopia and often require
1. Anterior chamber injuries are some of the surgical repair.
most frequently encountered sequelae of con- 5. Traumatic hyphema is treated on an outpa-
tusive ocular injury. tient basis unless follow-up or the application
2. Traumatic mydriasis is typically self-limited, of medications can not be assured (e.g. young
but occasionally can lead to chronic symptom- children).
atic glare and blurred vision. 6. Sickle cell screening should be performed on
3. Traumatic iritis is treated successfully with all African-American and African-Caribbean
cycloplegics. Steroid drops may be necessary patients with hyphema regardless of family
for significant inflammation. history.
85
Ocular trauma
7. Steroids, aminocaproic acid, and cycloplegics 13. Wachler BB, Krueger RR. Double-armed McCannell suture
are accepted medical treatments for hyphema. for repair of traumatic iridodialysis. Am J Ophthalmol
1996;122:109–110.
Anterior chamber washout with or without a
14. Oshika T, Amano S, Kato S. Severe iridodialysis from
trabeculectomy is necessary when medical phacoemulsification tip suction. J Cataract Refractive Surg
treatments fail to maintain an appropriate 1999;25:873–875.
intraocular pressure or corneal blood staining 15. Zeiter JH, Shin DH, Shi DX. A closed chamber technique for
occurs. repair of iridodialysis. Ophthal Surg 1993;24:476–480.
8. The mainstays for visualization of cyclodialy- 16. Bardak Y, Ozerturk Y, Durmus M, Mensiz E, Aytuluner E. Closed
chamber iridodialysis repair using a needle with a distal hole.
sis clefts are gonioscopy and, more recently,
J Cataract Refract Surg 2000;26:173–176.
ultrasound biomicroscopy. 17. Erakgun T, Kskaloglu M, Kayikcioglu O. A simple closed
9. Cyclodialysis resolution can be obtained with chamber technique for repair of traumatic iridodialysis in
cycloplegia, argon laser, or surgical repair and phakic eyes. Ophthal Surg Lasers 2001;31:83–85.
success is heralded by a severe yet transient 18. Chang S, Coll GE. Surgical techniques for repositioning a
elevation in intraocular pressure. dislocated intraocular lens, repair of iridodialysis, and
secondary intraocular lens implantation using innovative
25-gauge forceps. Am J Ophthal 1995;119:165–174.
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31. Rahmani B, Jahadi HR. Comparison of tranexamic acid and Ophthalmol 1967;78:714–721.
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randomized clinical trial. Ophthalmology 1999;106:375–379. glaucoma: a study of the after effects of traumatic hyphemas.
32. Kutner B, Fourman S, Brein K, et al. Aminocaproic acid Arch Ophthalmol 1964;72:39–44.
reduces the risk of secondary hemorrhage in patients 48. Tonjum AM. Intraocular pressure and facility of outflow
with traumatic hyphema. Arch Ophthalmol 1987;105(2): late after ocular contusion. Acta Ophthalmol 1968;46:886–
206–208. 908.
33. Crouch Jr. ER, Williams PB, Gray K, Crouch ER, Chames M. 49. Wolff SM, Zimmermann LE. Chronic secondary glaucoma
Topical amniocaproic acid in the treatment of traumatic associated with retrodisplacement of the iris root and
hyphema. Arch Ophthalmol 1997;115(9):1106–1112. deepening of anterior chamber angle secondary to
34. Pieramici DJ, Goldberg MF, Melia M, et al. A phase III, contusion. Am J Ophthalmol 1962;54:547–563.
multicenter, randomized placebo-controlled clinical trial of 50. Herschler J. Trabecular damage due to blunt anterior
topical aminocaproic acid (Caprogel) in the management segment injury and its relationship to traumatic glaucoma.
of traumatic hyphema. Ophthalmology 2003;110(11): Trans Am Acad Ophthalmol Otolaryngol 1977;83:239.
2106–2112. 51. Kaufman J, Tolpin D. Glaucoma after traumatic angle
35. Graul TA, Ruttum MS, Lloyd MA, Radius RL, Hyndiuk RA. recession. Am J Ophthalmol 1974;78:648–654.
Trabeculectomy for traumatic hyphema with increased 52. Thomas JV, Simmons RJ, Belcher CD III. Argon laser
intraocular pressure. Am J Ophthalmol 1994;117(2):155–159. trabeculoplasty in the presurgical glaucoma patient.
36. Belcher CD, Brown SV, Simmons RJ. Anterior chamber Ophthalmology 1982;89:187–191.
washout for traumatic hyphema. Ophthalmic Surg 53. Robin AL, Pollack IP. Argon laser trabeculoplasty in secondary
1985;16(8):475–479. form of open angle glaucoma. Arch Ophthalmol
37. Parrish RK, Baradino V Jr. Iridectomy in the surgical 1983;101:382–384.
management of eight ball hyphema. Arch Ophthalmol 54. Tesluk GC, Spaeth GL. The occurrence of primary open
1982;100:435–437. angle glaucoma in the fellow eye of patients with unilateral
38. Brodrick JD. Corneal blood staining after hyphaema. Br J angle-cleavage glaucoma. Ophthalmology 1985;92(7):
Ophthalmol 1972;56:589–593. 904–911.
39. Gottsch JD, Graham CR Jr, Hairston RJ, et al. Protoporphyrin 55. Mermound A, Salmon JF, Straker C, et al. Post-traumatic angle
IX photosensitization of corneal endothelium. Arch recession glaucoma: a risk factor for bleb failure after
Ophthalmol 1989;107:497–500. trabeculectomy. Br J Ophthalmol 1993;77:631–634.
40. Gottsch JD, Messmer EP, McNair DS, Font RL. Corneal 56. Manners T, Salmon, JF, Barron A, Willies, Murray AN.
blood staining: an animal model. Ophthalmology Trabeculectomy with mitomycin C in the treatment of post-
1986;93:797–802. traumatic angle recession glaucoma. Br J Ophthalmol
41. Nasrullah A, Kerr N. Sickle cell trait as a risk factor for 2001;85:159–163.
secondary hemorrhage in children with traumatic hyphema. 57. Chandler PA, Maumenee AE. A major cause of hypotony.
Am J Ophthalmol 1997;123:783–790. Am J Ophthalmol 1961;52:609–618.
42. Crouch ER Jr, Frenkel M. Aminocaproic acid in the 58. Aminlari A, Callahan CE. Medical, laser, and surgical
treatment of traumatic hyphema. Am J Ophthalmol 1976; management of inadvertent cyclodialysis cleft with hypotony.
81:355–360. Arch Ophthalmol 2004;122:399–403.
43. Edwards WC, Layden WF. Traumatic hyphema. Am J 59. Ormerod LD, Baerveldt G, Sunalp MA, Riekhof FT.
Ophthalmol 1973;75:110–113. Management of the hypotonous cyclodialysis cleft.
44. Rocha KM, Martins EN, Melo LA Jr, Bueno de Moraes NS. Ophthalmology 1991;98:1384–1393.
Outpatient management of traumatic hyphema in children: 60. Joondeph HC. Management of postoperative and
prospective evaluation. J AAPOS 2004;8:357–361. post-traumatic cyclodialysis clefts with argon laser
45. Wolff SM, Zimmerman LE. Chronic secondary glaucoma: photocoagulation. Ophthalmic Surg 1980;11:186–188.
association with retrodisplacement of iris root and deepening 61. Berinstein DM, Gentile RC, Sidoti PA, et al. Ultrasound
of the anterior chamber angle secondary to contusion. Am J biomicroscopy in anterior ocular trauma. Ophthalmic Surg
Ophthalmol 1962;84:547–563. Lasers 1997;28:201–207.
87
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62. Özdal MPC, Mansour M, Deschenes J. Ultrasound 68. Krohn J. Cryotherapy in the treatment of cyclodialysis
biomicroscopic evaluation of the traumatized eyes. cleft induced hypotony. Acta Ophthalmol Scand
Eye 2003;17:467–472. 1997;75:96–98.
63. Maumenee AE, Stark WJ. Management of persistent hypotony 69. Brooks AMV, Troski M, Gillies WE. Noninvasive closure of a
after planned or inadvertent cyclodialysis. Am J Ophthalmol persistent cyclodialysis cleft. Ophthalmology
1971;71:320–327. 1996;103:1943–1945.
64. Küchle M, Naumann GO. Direct cryopexy for traumatic 70. Alward WLM, Hodapp EA, Parel JM, Anderson DR. Argon laser
cyclodialysis with persisting hypotony: report in 29 endophotocoagulator closure of cyclodialysis clefts. Am J
consecutive patients. Ophthalmology 1995;102:322–333. Ophthalmol 1988;106:748–749.
65. Tate GW, Lynn JR. A new technique for the surgical repair of 71. Caronia RM, Sturm RT, Marmor MA, Berke SJ. Treatment of a
cyclodialysis induced hypotony. Ann Ophthalmol 1978;10: cyclodialysis cleft by means of ophthalmic laser
1261–1266. microendoscope endophotocoagulation. Am J Ophthalmol
66. Vannas M, Bjorkenheim B. On hypotony following 1999;128:760–761.
cyclodialysis and its treatment. Acta Ophthalmol 72. Delgado MF, Daniels S, Pascal S, Dickens CJ. Hypotony
1952;30:63–64. maculopathy: improvement of visual acuity after 7 years.
67. Viikari K, Tuovinen E. On hypotony following cyclodialysis 2001;32:931–933.
surgery. Acta Ophthalmol 1957;35:543–549.
88
7
Closed globe injuries: lens
David A. Goldman, Jennifer I. Hui
INTRODUCTION eyewall. Once this is complete, a careful system-

atic examination of the eye is performed.
Lens injuries have been reported to occur in 7– Evaluation of the crystalline lens is an integral
50% of eyes sustaining significant trauma.1–3 part of the examination in a traumatized eye.
Patients with traumatic lens injuries may present The position of the lens is fi rst determined. The
to the ophthalmologist immediately after sus- normal crystalline lens is held in place by the
taining an injury or at a much later time. Com- lens zonules (Figure 7.1). Partial dehiscence of Included
on DVD
plaints include decreased vision, fluctuating the lens zonules will lead to subluxation (Figure
vision, monocular diplopia, glare, or pain. In this 7.2). Subluxation implies the crystalline lens is
chapter we will discuss the history, evaluation, still held in place by the remaining lens zonules
and management strategies associated with but is no longer centered in the pupillary space.
traumatic lens injuries and potential long-term The elasticity of the remaining lens zonules pulls
sequelae. the lens away from the site of zonular dehis-
cence. Often this is detected by visualizing the
EVALUATION curvilinear lens equator when the pupil is dilated.
Complete zonular dehiscence leads to lens dis-
History is invaluable when approaching trau- location (Figure 7.3). A dislocated lens most
matic lens injuries. The examiner must deter- frequently falls into the vitreous cavity, but
mine the time and mechanism of injury as well occasionally can prolapse forward into the ante-
as the timing, quality, and nature of the symp- rior chamber. While a subluxated lens may be
toms. In particular, the mechanism of injury will asymptomatic if minimally decentered, com-
help guide the examination and raise or lower plete dislocation of the lens into the vitreous
the suspicion of a possible eyewall violation or cavity always leads to immediately decreased
intraocular foreign body. It is not uncommon for vision, as the eye is functionally aphakic. Contu-
patients with traumatic cataracts to present with sive ocular injury can also cause diffuse damage
a remote history of trauma or sometimes a nega- of the lens zonules leading to instability of the
tive history altogether. Past ocular history, such lens and phacodonesis. Phacodonesis may range
as previous surgery, is also an essential part of from minimal shimmer of the crystalline lens to
the evaluation. frank, profound movement of the lens–iris dia-
A thorough examination of the eye, as dis- phragm. To test for phacodonesis, the patient is
cussed in Chapter 3, is mandatory following any asked to look away from the slit lamp beam and
ocular trauma. Lens injury frequently coexists then rapidly return gaze to the light. Gently
with other significant ocular injuries. A screen- pounding the slit lamp table with a closed fist
ing slit lamp examination is performed before while the patient looks straight ahead can some-
eye drops are instilled or intraocular pressure is times produce similar results. Any movement of
taken in order to determine the integrity of the the lens is attributable to zonular weakness and
89
Ocular trauma
Visual axis Intact zonules body but clinical suspicion remains high, a CT
scan must be obtained. Additionally, CT may aid
in determining the nature of the foreign body
(metallic vs. nonmetallic). MRI should not be
utilized if a foreign body is suspected as there is
a risk of migration with objects that are metallic
in nature.
Trauma to the lens may cause various types of
opacities as discussed below. The lens should be
examined under direct illumination and retro-
illumination to determine the presence and loca-
tion of lens opacities. The anterior and posterior
subcapsular areas are the most common sites
of traumatic cataract. Although cataracts may
not be present on initial presentation, they can
rapidly progress in hours to days depending on
the extent of injury and the integrity of the lens
capsule.
Under circumstances in which examination of
the lens is prohibited secondary to hyphema,
Crystalline lens corneal disease, or anterior segment disruption,
Figure 7.1 Diagrammatic representation of the normal an imaging modality may be pursued. Options
anatomic position of the crystalline lens supported 360
include B-scan ultrasound, ultrasound biomicro-
degrees by the lens zonules (iris not pictured).
scopy, CT, or MRI. CT and MRI may provide
important information about the lens and the
should be documented at the time of initial orbit, but are seldom indicated solely for locating
examination. Other signs that are indicative of the lens. Ultrasound is more efficient and quickly
zonular weakness and often coexist with all obtained and may be performed in an office
three of these conditions include iridodonesis, setting. When the view through the anterior
asymmetric anterior chamber depth (the affected segment is clear and the lens is not visualized,
side typically has the deeper chamber), an eccen- one must consider complete dislocation of the
tric pupil, or the presence of vitreous at the lens into the vitreous cavity or through a site of
pupillary margin or within the anterior chamber scleral rupture.1
(Figure 7.4).
If a corneal or anterior scleral laceration is DIAGNOSIS AND TREATMENT
present, the examiner must carefully look for iris
transillumination defects, a disruption in the General considerations
anterior capsule or the presence of an intralen- While initial trauma to the lens may appear insig-
ticular foreign body. With an anterior laceration nificant, delayed sequelae may present days to
and a violated lens capsule, the patient is assumed months after the initial incident. These sequelae
to have an intraocular foreign body until proven are discussed below and are arranged in order of
otherwise. If ultrasound fails to reveal a foreign when they would most likely present after the
90
Broken zonules Visual axis
A B
Subluxated lens
Figure 7.2 (A) Diagrammatic representation of lens subluxation (iris not pictured). Focal dehiscence of lens
zonules causes subluxation away from the dehiscence. (B) Traumatic lens subluxation.
initial injury, ranging from immediate (lens dis- by the intact zonules. The anterior chamber
location) to delayed by months or years (phaco- is often asymmetrically deep in this setting.6
lytic glaucoma). The specific treatment modalities B-scan ultrasound or ultrasound biomicroscopy
for each injury type are described in detail. may aid in localization of the lens in eyes with
a suboptimal view of the anterior chamber.7,8
Lens subluxation and dislocation If the lens cannot be visualized, extraocular
(immediate to delayed) displacement of the lens is also a consideration,
Lens subluxation or dislocation, found alone or especially in patients with a history of large-
in conjunction with other ocular injuries, is most incision surgery (e.g. extracapsular cataract
frequently caused by trauma.4 Lenticular sublux- extraction, penetrating keratoplasty). The lens
ation is not always evident with the traditional may have extruded through a previous surgical
slit lamp examination. For example, an inferior wound or another site of structural disruption.
zonular disruption may not be evident unless the Scleral ruptures are not always visible and an
patient is in a supine position. Thus, a lens with extruded crystalline lens may be found in a sub-
zonular weakness can change its position depend- conjunctival location. 9 Scleral ruptures most fre-
ing on the posture of the patient.5 If zonular quently occur between the limbus and the spiral
disruption is incomplete, the lens is typically of Tillaux in the superonasal and superotempo-
drawn away from the site of the zonular rupture ral quadrants. Lenses in the subconjunctival
91
Ocular trauma
Visual axis
Sclera Corneal limbus
A B
Broken lens Dislocated

zonules lens
Figure 7.3 (A) Diagrammatic representation of lens dislocation. Total zonular dehiscence leads to lens dislocation
(typically posteriorly). (B) A mature cataract is seen floating in the inferior vitreous cavity many years after a
contusive injury to the eye.
A B
Figure 7.4 Vitreous is seen in the anterior chamber (A) after a 50-year-old woman was struck with a thrown can of
tuna during a domestic dispute. The crystalline lens was visible on the surface of the retina (B). No inflammation
was present. Aphakic correction was provided with a contact lens and the dislocated lens was serially observed.
92
space are usually absorbed, though calcium

deposits may remain.10 Suspicion for a globe
rupture should be raised in cases of hypotony or
circumferential subconjunctival hemorrhage fol-
lowing contusive injury to the eye.
Symptoms from a subluxated crystalline lens
correlate with the degree of subluxation and
cataract formation. The lens creates astigmatism
when it is displaced from its normal anatomic
location. Increasing amounts of zonular disrup-
tion result in progressive spherical shape and
Figure 7.5 Traumatic anterior lens dislocation with
secondary myopic lens changes.11 Monocular diffuse contact between the corneal endothelium and
diplopia is induced if the lens margin splits the the crystalline lens.
visual axis.
Rapid, severe vision loss results from posterior block is often induced given the limited space in
dislocation of the lens as the eye becomes func- the anterior chamber (Figure 7.5). Initial treat-
tionally aphakic. Visual acuity can often be ment with anti-inflammatories and glaucoma
improved with spectacles or a contact lens. A medications is initiated in preparation for defi ni-
contact lens may provide the most noteworthy tive surgery. Corneal–lenticular touch imparts a
relief of symptoms as it reduces the amount of significant risk of endothelial dysfunction and
induced anisometropia that occurs with mono- subsequent corneal decompensation. Dilation is
cular aphakic spectacle correction. Symptoms not recommended as the lens may dislocate into
may also be minimized with miotics to prevent the vitreous and require a vitrectomy for removal.
pupillary dilation. Medical management of sub- Since most injuries occur in young patients, the
luxated or dislocated lenses is often preferable to crystalline lens is often not cataractous and can
surgical options. Extraction of a subluxated cata- be readily aspirated once the capsular bag is
ract is fraught with difficulties depending on opened. If the lens is cataractous, phacoemulsi-
the degree of subluxation. Severely subluxated fication can be attempted. The cornea must be
lenses with vitreous prolapse are often referred to relatively clear and the anterior chamber of
vitreoretinal specialists for pars plana vitrectomy sufficient depth to ensure safe removal. In both
and lensectomy. With milder degrees of subluxa- instances, viscoelastic is used to push the ante-
tion, the use of capsular hooks and/or capsular rior vitreous back to prevent inadvertent vitreous
tension rings can stabilize the lens so that routine traction. If vitreous presents, an anterior vitrec-
phacoemulsification with posterior chamber in- tomy is performed following cataract removal.
traocular lens implantation may be performed. An anterior chamber or sutured posterior
Intracapsular cataract surgery with anterior cham- chamber intraocular lens may be implanted at
ber intraocular lens implantation is advocated by the time of cataract extraction if the inflamma-
some for severely subluxated cataracts without tion is sufficiently treated. If severe inflamma-
vitreous prolapse. Surgeon experience will dictate tion is present, the eye is often left aphakic.
the appropriate removal strategy. Secondary intraocular lens implant can be per-
Traumatic lens dislocation into the anterior formed when the inflammation subsides. If the
chamber causes a severe loss of vision. Pupillary anterior chamber is not sufficiently deep, the
93
Ocular trauma
cataract is dense, small incision cataract surgery several days so the surgery can be performed in
is not possible, or significant vitreous prolapse is a noninflamed and normotensive eye. Routine
present preoperatively, intracapsular extraction phacoemulsification with posterior chamber
or pars plana vitrectomy and lensectomy is intraocular lens implantation can often be per-
indicated. formed depending on the mechanism of injury
The crystalline lens is more frequently dislo- and the amount of capsular disruption.
cated posteriorly into the vitreous cavity. Patients
have significant visual symptoms secondary to Traumatic cataract (days to years)
functional aphakia. The status of the lens capsule Cataracts may arise from contusive eye trauma
plays a vital role in determining appropriate treat- immediately after injury or many years later.
ment. If the capsule is intact, the lens may remain They are reported to occur in 11% of eyes with
in the vitreous cavity without inciting inflamma- closed globe injuries.2 The concept of ‘coup’ and
tion. A violated capsule frequently leads to a ‘contrecoup’ forces was fi rst described by Wolter12
variable inflammatory response requiring sur- and Weidenthal and Schepens.13 These forces,
gical lens removal after an initial course of anti- in addition to equatorial expansion of the globe,
inflammatories. A vitreoretinal surgeon provides are the postulated mechanisms of injury. ‘Coup’
defi nitive surgical care. Most lenses are removed refers to direct forces while ‘contrecoup’ refers
by phacofragmentation through the pars plana to injury occurring as a result of transmitted
after a vitrectomy has been performed. If the lens shock waves through the lens. Equatorial expan-
is too dense for phacofragmentation within the sion of the globe occurs when it is shortened in
vitreous, it may be brought into the anterior the anteroposterior direction at the time of
chamber and removed through a limbal wound.6 impact. Such expansion may result in lens cap-
sular rupture, zonular dehiscence, or both.14
Phacoanaphylactic uveitis (hours to years) Cataracts can form following disruption of the
Phacoanaphylactic uveitis is a rare, aggressive lens capsule. A capsular defect allows aqueous
immune response mounted against exposed lens humor to enter the lens, leading to increasing
proteins following traumatic lens capsule disrup- opacity until the flow of aqueous ebbs.15 The
tion. It is frequently associated with chemosis, natural history of lens capsule violation is unclear.
conjunctival injection, anterior chamber cell and The anterior capsule has a high capacity for
flare, large and multiple keratic precipitates, and healing because of the regenerative properties of
in severe cases, hypopyon. Rarely, the fellow eye the subcapsular epithelium and is less suscepti-
may develop similar inflammation. Typically, the ble to rupture given its greater thickness. If the
intraocular pressure is low; however, elevations capsular defect is <2 mm, the epithelium rapidly
can also occur (see Lens-induced glaucoma, restores continuity. Defects larger than 3 mm
below). Elevated intraocular pressure may be frequently lead to lenticular opacity. Healing of
reduced with topical beta-blockers, carbonic the capsule limits passage of free ions and fluid
anhydrase inhibitors, alpha-adrenergic blockers that may lead to cataract formation. The anterior
or prostaglandin analogues. Intraocular inflam- capsule may also spontaneously reopen, causing
mation may be alleviated with steroids, either severe inflammation and secondary glaucoma
topically, via sub-Tenon’s injection, or orally. days to months following injury.
Removal of the lens, however, is the defi nitive Most traumatic cataracts are not associated
required treatment. Surgery is often deferred for with capsular disruption. An ocular contusion
94
Figure 7.6 Classic petalloid anterior subcapsular

cataract (‘sunflower cataract’) seen in retroillumination.
Figure 7.7 Mature cataract following a fireworks

most commonly produces a ‘sunflower cataract,’ explosion near the right eye of an 11-year-old child.
one that is localized to the anterior or posterior Capsular wrinkling is present temporally. Concomitant
subcapsular cortex and consists of radiating iris injury is visible as a D-shaped iris deformity.
spokes (Figure 7.6).15
Traumatic cataracts, if not removed, have a The location of the cataract within the lens itself
predisposition to progress to mature cataracts also plays a role with respect to symptomatology.
(Figure 7.7), often precluding a view of the Posterior subcapsular cataracts generally produce
posterior pole. Patients usually present with more symptoms than nuclear sclerotic or cortical
decreased vision, and, rarely, intraocular inflam- cataracts of comparable density. Unless the
mation and elevated pressure (see Lens-induced cataract interferes with a patient’s activities of
glaucoma, below). It is important to determine daily living or is associated with intraocular
the state of the posterior segment. The patient’s inflammation, infection, or glaucoma, it is often
visual potential and the presence of posterior best managed with observation.
pathology are important factors to consider when Preoperatively, the eye must be thoroughly
planning the surgical approach. If a patient pres- examined to determine the presence and degree
ents with a total cataract, B-scan ultrasound is of phacodonesis, vitreous prolapse, and the state
used to explore the possibility of retinal tear or of the posterior capsule. In general, phacoemulsi-
detachment, choroidal rupture or occult intra- fication is often the most convenient route of cat-
ocular foreign body. aract removal. Great caution must be utilized in
The degree and location of cataract formation cases of suspected zonular instability. Newer
impacts the timing of surgical removal. The technologies, including capsular tension rings
presence of cataract does not always require sur- and capsular fi xation hooks, have greatly improved
gical removal. If the cataract is not significantly the ability to remove these tenuous lenses via
dense or does not involve the central visual axis, an anterior approach. Additionally, advanced
patients may experience relatively few symp- hemodynamic parameters on new phacoemulsi-
toms. Refraction often improves visual acuity. fication units allow safe removal of traumatic
Cataracts do not necessarily progress and are not cataracts with phacoemulsification.1,18,19 A
always associated with other ocular injuries.16,17 continuous infusion can be utilized to prevent
95
Ocular trauma
shallowing of the anterior chamber and worsen- tion of a cataractous lens offers many advantages:
ing of vitreous prolapse. Capsular dyes such as it eliminates the source of late inflammation
indocyanine green or trypan blue are used to and increased intraocular pressure and allows
assist in performing a capsulorhexis when the red earlier visual rehabilitation. Disadvantages in-
reflex is absent. If phacoemulsification is not pos- clude increased short-term postoperative inflam-
sible due to lens brunescence, an extracapsular mation, increased risk of intraoperative bleeding
extraction may be required. and the possibility that the cataract may not have
If the capsule is not intact or there is a significant become visually significant.2
degree of phacodonesis or subluxation, other Young children present a unique challenge
methods of cataract removal must be considered. given their risk of amblyopia. If pediatric
The route of removal depends largely on the cataract extraction is undertaken, many factors
experience of the surgeon. If an anterior approach require consideration. One of these concerns is
is not felt to be safe, vitreoretinal consultation is the propensity for children to develop posterior
recommended for defi nitive management. Com- capsular opacifications relatively soon after cata-
bined pars plana lensectomy and vitrectomy are ract removal.21,22 For this reason, a primary pos-
implemented with increasing frequency.20 The terior capsulotomy and anterior vitrectomy are
infusion port should be placed away from the site recommended at the time of cataract extraction
of any choroidal or retinal detachment. Perfluoro- for children not mature enough to cooperate
carbons can aid in mobilizing posteriorly dis- with a YAG laser capsulotomy (typically less
located lens fragments, supporting fragments than 6 years of age). Once determined to be the
during their removal, and protecting the retina.6 treatment of choice, cataract extraction should
Although rarely performed, intracapsular cata- be expedited to minimize disruptions in physi-
ract surgery is an option if significant zonular ologic and anatomic ocular development.
instability is present and the vitreous face is intact. Pediatric intraocular lens implantation is also
Surgeon experience plays an important role in the controversial. Of note, one study demonstrated
decision-making process. a 70% rate of visual acuity of >20/60 in children
Primary intraocular lens implantation may be with intraocular lens implantation (136 children
considered after any method of cataract extrac- between 2 and 16 years of age, one child less than
tion if inflammation is well controlled and the 2 years of age). Aphakia is generally recom-
risk of infection is deemed to be low. The lens mended for children younger than 2 years of
may be placed in the capsular bag, the sulcus, age,23 although intraocular implantation at
the anterior chamber or fi xated to the iris or younger ages is becoming more common.
sclera. If placed in the capsular bag, the haptics Ocular trauma with associated cataract is often
should be placed perpendicular to any zonular correlated with poor outcomes secondary to
defect for maximal capsular bag stabilization and posterior segment abnormalities including retinal
expansion.1 detachment, macular scarring, and traumatic
The timing of cataract removal depends on optic neuropathy. Between 50% and 70% of in-
many factors including the degree of inflamma- jured eyes have been reported to have significant
tion, need for visual rehabilitation (monocular posterior segment injuries.2,24 Preoperative
patient or a child of amblyogenic age), the need factors associated with poor visual outcomes
for further ocular procedures and the general include an afferent pupillary defect or
medical condition of the patient. Primary extrac- iridodialysis.24
96
CASE EXAMPLES
Case report: traumatic cataract (Figure 7.8)

A 3-year-old girl complained to her mother of severe Topical anti-inflammatories and antibiotics were ini-
pain and decreased vision in her left eye. Her family tiated and the patient was scheduled for surgery.
rushed her to the emergency room for evaluation. During the surgery, trypan blue was used to stain the
After initial stabilizing treatment from an ophthal- anterior lens capsule to aid in visualization (B). After
mologist, the patient’s care was transferred to the the lens material was aspirated through the pre-
eye clinic for definitive evaluation and management. existing anterior capsular violation (white arrow, C),
Three days after the initial injury, visual acuity in the it was evident that the penetrating injury involved a
left eye was hand motions. Slit lamp examination small portion of the peripheral posterior capsule as
revealed a Seidel negative corneal laceration of the well (black arrow, C). The posterior capsular defect
superotemporal cornea (black arrow, A). The anterior was round and under no tension. The anterior cap-
lens capsule was violated with cataractous lens sular break was converted into a capsulorhexis and
material protruding through the defect. An ultra- a one-piece acrylic intraocular lens was injected into
sound was performed which showed no intraocular the capsular bag with the haptics directed away
foreign body or posterior segment pathology. from the pre-existing posterior capsular break.
A B
Included
on DVD
C D
97
Ocular trauma
Case report: traumatic cataract (cont’d)

Because of the likelihood of future posterior capsular performed via the pars plana (D). The patient recov-
opacification and the patient’s age and inability to ered uneventfully with a final best-corrected visual
participate in a YAG laser capsulotomy, a posterior acuity of 20/20. Continued follow-up with a pediatric
capsulotomy and limited anterior vitrectomy were ophthalmologist was arranged.
Lens-induced glaucoma (days to years)

Lens-induced glaucoma may be precipitated by
ocular trauma. The presentation varies by mech-
anism (open angle vs. closed angle), time frame
(immediate vs. delayed), and capsular status
(intact vs. violated). Specific diagnostic entities
include:
1. phacolytic glaucoma: open angle, delayed Included
on DVD
onset, intact capsule

2. lens particle glaucoma: open angle, usually
rapid onset, violated capsule
3. phacoanaphylactic glaucoma: open angle,
variable onset, violated capsule
Figure 7.9 A 62-year-old female with a remote history
4. phacomorphic glaucoma: closed angle, usually of trauma presented with severe pain and redness in an
delayed onset, intact or violated capsule. eye with a longstanding history of poor vision. Vision
Ocular trauma is a common precipitating was light perception and intraocular pressure was
factor in mature or hypermature cataracts, severely elevated. The video capture shows corneal
although the trauma is often remote. Phacolytic edema, anterior chamber debris with a hypopyon, and
a hypermature cataract. Cataract surgery with
glaucoma is a secondary open angle glaucoma
intraocular lens implantation was successful, and final
resulting from leakage of lens proteins through visual acuity was 20/25.
the intact capsule of a hypermature cataract
(Figure 7.9). Intraocular pressure increases
in response to lenticular proteins and protein- unlike phacomorphic glaucoma, the anterior
laden macrophages occluding the trabecular chamber angle is open. Inflammatory cells
meshwork.25 The proteins are generally of and proteinaceous debris are visible within
high molecular weight. Characteristic clinical the aqueous but large keratic precipitates
features include white patches on the anterior are not typically seen. Corneal edema may
lens capsule and small white collections of hinder slit lamp examination of the anterior
inflammatory debris circulating within the chamber.
anterior chamber.26 Patients frequently pre- Lens particle glaucoma can occur following
sent with pain and redness in an eye with a ocular trauma if the capsular bag is violated.
history of slow, progressive visual decline. Intraocular pressure is elevated when lens parti-
On slit lamp examination the anterior chamber cles exit the confi nes of the capsular bag and
may be slightly shallowed secondary to an mechanically block the trabecular meshwork.
enlarged anterior–posterior lens diameter, but Mild to moderate inflammation is typically seen.
98
Conversely, phacoanaphylactic glaucoma occurs glaucoma once the initial inflammatory episode
in similar situations, but is associated with a is controlled.
severe, granulomatous inflammatory reaction. For all lens-induced glaucomas, medical man-
Mutton fat keratic precipitates and posterior syn- agement is initially instituted in an effort to
echiae are common, and a hypopyon is occasion- decrease intraocular inflammation and pressure.
ally seen. The anterior chamber angle is open in In the acute phase, intravenous osmotic agents
both entities. such as mannitol or oral osmotic agents such as
Phacomorphic glaucoma is a form of secondary isosorbide and glycerin are utilized to lower
angle closure. A mature cataract is elongated the pressure. Oral acetazolamide, topical beta-
axially and may cause pupillary block or second- blockers, topical carbonic anhydrase inhibitors,
ary angle closure if the lens apparatus is and topical alpha-adrenergic blockers are used
sufficiently displaced anteriorly. Patients present to maintain a normal intraocular pressure. In
with pain and redness in an eye that demon- general, miotics are not recommended as they
strates corneal edema, a shallow anterior may worsen or induce angle closure via forward
chamber, and a dense cataract with increased rotation of the lens–iris diaphragm. Surgical
lens thickness on slit lamp examination.27 Mild intervention is typically deferred until inflam-
to moderate inflammation is often present. mation is controlled and intraocular pressure
Initial treatment includes anti-inflammatories decreases. However, if either persists, removal of
and medication to lower intraocular pressure. the cataractous lens is the defi nitive treatment
A laser peripheral iridotomy may be placed in of choice. Intraocular lens implantation may be
an attempt to relieve any pupillary block that delayed if intraocular inflammation has not been
may be present. However, cataract extraction adequately controlled, although this is rarely the
is the defi nitive treatment for phacomorphic case.
99
Ocular trauma
CASE EXAMPLES
Case report: lens particle glaucoma (Figure 7.10)

A 31-year-old male presented to the emergency oscopy. The patient underwent primary closure of
room with pain in his left eye after cutting a tree with the corneal laceration (B). Cultures of the aqueous
a machete without using protective eyewear. He did not reveal growth. Within weeks, the patient
recalled being hit in the face with a frond from a developed elevated intraocular pressure, increased
palm tree. His visual acuity was 20/20 and 20/80, and cell and flare, and white fluffy lenticular material was
intraocular pressures were 18 and 12 without a rela- noted in the anterior chamber (C). A diagnosis of
tive afferent pupillary defect. On slit lamp examina- lens particle glaucoma was made. Intensive anti-
tion a stellate corneal laceration was noted in the inflammatory treatment was started and cataract
central cornea (Seidel positive) associated with 2+ surgery was scheduled. The cataract was removed
anterior chamber cell and flare. A defect in the ante- the next day, topical steroids were continued, and
rior lens capsule with a sectoral traumatic cataract his pressure quickly returned to the normal range.
was also noted (A). A small amount of pigmented On the final follow-up visit, a well-centered intra-
material was noted on the anterior lens surface. No ocular lens was present (D) and visual acuity was
foreign bodies were noted within the angle on goni- 20/20.
A B
C D
100
SUMMARY 6. Marcus DF, Topping TM, Frederick AR. Vitreoretinal

management of traumatic dislocation of the crystalline lens.
Int Ophthalmol Clin 1995;3591:139–150.
1. Lens subluxation implies a partial dehiscence
7. Berinstein DM, Gentile RC, Sidoti PA, et al. Ultrasound
of zonules whereas lens dislocation is caused biomicroscopy in anterior ocular trauma. Ophthalmic Surg
by complete zonular dehiscence. Lasers 1997;28:201–207.
2. Phacodonesis is a pathologic instability of the 8. Ozdal MPC, Mansour M, Deschenes J. Ultrasound
lens caused by diffuse zonular damage. biomicroscopic evaluation of the traumatized eye.
3. Traumatic lens instability is often accompa- Eye 2003;17:467–472.
9. Sathish S, Chakrabarti A, Prajna V. Traumatic subconjunctival
nied by an asymmetrically deep anterior
dislocation of the crystalline lens and its surgical
chamber, iridodonesis, an eccentric pupil management. Ophthalmic Surg Laser 1999;30:684–686.
shape, or vitreous prolapse. 10. Yurdakul NS, Ugurlu S, Yilmaz A, Maden A. Traumatic
4. The urgency of traumatic cataract removal subconjunctival crystalline lens dislocation. J Cataract Refract
depends on the presence of visual symptoms, Surg 2003;29:2407–2410.
inflammation, elevated intraocular pressure, 11. Ellant JP, Obstbaum SA. Lens-induced glaucoma.
Doc Ophthalmol 1992;81:317–338.
and ability to follow up.
12. Wolter JR. Coup-contrecoup mechanism of ocular injuries.
5. Removal techniques for traumatic cataracts Am J Ophthalmol 1963;56:785–796.
vary depending on zonular stability, presence 13. Weidenthal DT, Schepens CL. Peripheral fundus changes
of vitreous prolapse, cataract density, and associated with ocular contusion. Am J Ophthalmol
surgeon preference. 1966;62:465–477.
6. Traumatic lens sequelae may occur years after 14. Shingleton BJ, Hersch PS, Kenyon KR, eds. Eye Trauma.
St. Louis, MO: Mosby-Year Book; 1991; Ch. 11, Lens injuries,
the initial injury.
pp. 126–135.
7. Traumatic lens injuries can induce glaucoma 15. Trevor-Roper PD. The eye and its disorders. The lens.
via multiple open and closed angle mecha- Int Ophthalmol Clin 1974;14:485–520.
nisms, but lens removal is the defi nitive man- 16. Yasukawa T, Kita M, Honda Y. Traumatic cataract with a
agement for each entity. ruptured posterior capsule from a nonpenetrating ocular
injury. J Cataract Refract Surg 1998;24:868–869.
17. Saika S, Kin K, Ohmi S, Ohnishi Y. Posterior capsule rupture
REFERENCES
by blunt ocular trauma. J Cataract Refract Surg
1997;23:139–140.
1. Mian SI, Azae DT, Colby K. Management of traumatic 18. Cionni RJ, Osher RH. Management of profound zonular
cataracts. Int Ophthalmol Clin 2002;42:23–31. dialysis or weakness with a new endocapsular ring designed
2. Kuhn F, Mester V. Anterior chamber abnormalities for scleral fixation. J Cataract Refract Surg 1998;24:1299–1306.
and cataract. Ophthalmol Clin North Am 2002;15: 19. Menapace R, Findl O, Georgopoulos M, Rainer G, Vass C,
195–203. Schmetterer K. The capsular tension ring: designs,
3. Lamkin JC, Azar DT, Mead MD, Volpe NJ. Simultaneous applications, and techniques. J Cataract Refract Surg
corneal laceration repair, cataract removal, and posterior 2000;26:898–912.
chamber intraocular lens implantation. Am J Ophthalmol 20. Chaudhry NA, Belfort A, Flynn HW, Tabandeh H, Smiddy WE,
1992;113:626–631. Murray TG. Combined lensectomy, vitrectomy and scleral
4. Jones LD, Sampat V, Hero M. Indirect trauma causing fixation of intraocular lens implant after closed-globe injury.
dislocation of the crystalline lens: a case report. Eur J Ophthalmic Surg Lasers 1999;30:35–81.
Ophthalmol 2003;13:91–92. 21. Chrousos GA, Parks MM, O’Neill JF. Incidence of chronic
5. Loo AV, Lai JS, Tham CC, Lam DS. Traumatic subluxation glaucoma, retinal detachment and secondary membrane
causing variable position of the crystalline lens. J Cataract surgery in pediatric aphakic patients. Ophthalmology
Refract Surg 2002;28:1077–1079. 1984;91:1238–1241.
101
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22. Keech RV, Cibis-Tongue A, Scott WE. Complications after secondary to ocular contusion injuries. Retina
surgery for congenital and infantile cataracts. Am J 2002;22:575–580.
Ophthalmol 1989;108:136–141. 25. Filipe JC, Palmares J, Delgado L, Lopes JM, Borges J, Castro-
23. Krishnamachary M, Rathy V, Gupta S. Management of Correia J. Phacolytic glaucoma and lens-induced uveitis.
traumatic cataract in children. J Cataract Refract Surg Int Ophthalmol 1993;17:289–293.
1997;23:681–687. 26. Epstein DL. Diagnosis and management of lens-induced
24. Greven CM, Collins AS, Slusher MM, Weaver RG. Visual results, glaucoma. Ophthalmology 1982;89:227–230.
prognostic indicators, and posterior segment findings 27. De Leon-Ortega JE, Girkin CA. Ocular trauma-related
following surgery for cataract/lens subluxation-dislocation glaucoma. Ophthalmol Clin N Am 2002;15:215–223.
102
8
posterior segment
John J. Miller, Krista D. Rosenberg
INTRODUCTION 1. Trauma contributes to the peak incidence in

younger years (20–29 years of age).
Contusive ocular injury may damage posterior 2. 80% of traumatic detachments occur prior to
segment structures by multiple mechanisms. In- the age of 40.
jury severity varies widely from self-limited peri- 3. Men outnumber women in traumatic detach-
pheral commotio retinae to vision-threatening ment (78% vs. 22%).
retinal detachment. The vitreoretinal interface 4. Non-traumatic detachments contribute to the
plays a vital role in the pathophysiology of most second peak incidence between the ages of 60
retinal injuries. Retinal detachment is often the and 69.
fi nal common pathway for traumatic disruption 5. 75% of non-traumatic detachments occur
of the pars plana, vitreous base, or retina. In this after the age of 39.
chapter we will discuss the epidemiology, patho- The increased risk of non-traumatic detachment
physiology, examination, and treatment of con- in myopic patients is well established. While
tusive posterior segment injury. Many of the some studies were unable to reach a conclusion
entities described here can occur with open globe regarding the role of myopia in traumatic detach-
injuries; however, in these cases repair of the ments,5 others concluded that myopia was indeed
globe violation remains the primary goal of initial a risk factor. While 3% of the general population
management (see Chapter 11). Treatment of has myopia of 2.5 diopters or greater, 28% of
coexisting posterior segment injuries following traumatic detachments have this degree of
primary closure of an open globe injury typically myopia or more. Assuming that myopes have a
requires management by a vitreoretinal special- similar trauma incidence as hyperopes and
ist. Such complex injuries are outside the scope of emmetropes, the incidence of traumatic retinal
this chapter. detachments in myopes may be as much as nine
times greater.
Trauma, in addition to proliferative diabetic
EPIDEMIOLOGY retinopathy and retinal tear, is a leading cause of
vitreous hemorrhage.6–8 Vitreous hemorrhage
Much of the reported epidemiologic information occurs in approximately 19% of all posterior
regarding contusive posterior segment injury segment injuries9 and is most commonly associ-
focuses on traumatic retinal detachment, a fi nal ated with contusive (66%), projectile (25%),
common pathway for most posterior segment and lacerating (9%) injuries. Trauma is the most
injuries. Traumatic retinal detachments account common cause of unilateral vitreous hemorrhage
for 10% and 19% of all phakic retinal detach- in patients under 40 years of age, usually occur-
ments.1–4 Phakic retinal detachments have been ring in males.
noted to have a bimodal distribution and several Traumatic choroidal ruptures have been
distinct clinical characteristics: reported in 4–10% of contusive ocular
103
Ocular trauma
injuries.10,11 Closed globe trauma from motor forces on the vitreoretinal interface that shear
vehicle accidents, assault,12 sports-related activi- vessels may also disrupt the normal retinal archi-
ties,13 forceps delivery,14 and paintball injuries15 tecture (e.g. macular hole).
are all reported causes of choroidal rupture. Weidenthal and Schepens described the mech-
anisms of traumatic tear formation by studying
PATHOPHYSIOLOGY pig eyes subjected to pellet gun injury. Most
peripheral retinal damage occurred from rapid
Contusive injuries to the eye cause deformation equatorial scleral expansion and rotation, while
of normal ocular architecture and, at times, dis- the vitreous and retina are pulled away from the
ruption of the vitreoretinal interface. The vitre- underlying pigment epithelium.16 Contusive
ous most tightly adheres to the retina at the ocular trauma can disrupt normal vitreoretinal
vitreous base, a band of condensed vitreous that adhesions and may cause retinal dialyses, giant
straddles the ora serrata 360 degrees (Figure retinal tears, horseshoe retinal tears, or tears in
8.1). Firm vitreoretinal adherence is also present the nonpigmented pars plana epithelium. Tears
along the retinal vasculature and at the optic in the nonpigmented pars plana epithelium are
nerve head. Vitreous hemorrhage is caused by much less common and are caused by traction at
traction or shearing of a normal or abnormal the anterior aspect of the vitreous base. A retinal
retinal vessel, frequently when traumatic separa- dialysis occurs when vitreous base traction causes
tion of the vitreous occurs. The rapid tractional a disinsertion of retina from the nonpigmented
pars plana epithelium at the ora serrata, rather
than a tear within the retina. The vitreous
Pars plan Ora serrata
remains attached in cases of pars plana tears and
retinal dialyses. Such clinical scenarios are more
common following contusive trauma in young
patients with an intact, formed vitreous. Giant
retinal tears are created when broad areas of
Vitreous base vitreoretinal adherence posterior to the ora
insertion serrata are placed under traction. Vitreous
remains attached to the anterior lip of the giant
tear while posterior vitreous detachment allows
free mobility of the posterior retinal lip. Horse-
shoe tears are created when a focal area of vit-
reoretinal adherence is placed under traction by
a surrounding vitreous detachment. This clinical
Retina scenario commonly occurs in older patients with
an evolving posterior vitreous detachment.
A few generalizations can be made regarding
Figure 8.1 Anatomical interaction of the vitreous the origins of retinal detachments and their pos-
base and ora serrata. The vitreous base extends
sible relationship to trauma. Most retinal dialy-
approximately 2 mm anterior to the ora serrata and 2–
4 mm posteriorly. This tight interface plays a major role ses and giant retinal tears are related to trauma,
in the pathophysiology of traumatic retinal breaks and although some develop without trauma. Detach-
detachments. ments related to superior or nasal dialyses, pars
104
Closed globe injuries: posterior segment
plana tears, vitreous base avulsions, and necrotic an open globe. Examination considerations for a
retinal holes may be assumed to be of traumatic potential open globe are covered in Chapter 11.
origin, even if the history of trauma is remote or Any hyphema should be noted. Intraocular pres-
not recalled by the patient. Conversely, most sure should be measured after confi rmation of
horseshoe tear-related detachments are not asso- globe integrity.
ciated with contusive trauma. After the pupils have been pharmacologically
Choroidal ruptures occur when contusive dilated, evaluate the lens for traumatic lens opac-
forces overcome the inelastic nature of Bruch’s ities (cataract) and traumatic lens instability
membrane and the retinal pigment epithelium (phacodonesis). Both indicate significant ocular
(RPE), causing a tear in these tissues. Histo- trauma and often coexist with disruption of the
pathologic evidence reveals an intact overlying vitreous base and retina. With the slit lamp bio-
retina with variable fibroglial scarring.17 microscope, examination of the anterior vitreous
just posterior to the lens yields clues to vitreo-
EXAMINATION AND DIAGNOSIS retinal integrity. The presence of liberated retinal
pigment epithelial cells and pigment-containing
Clinical examination in the setting of ocular macrophages (also known as tobacco dust or Included
on DVD
trauma must be tailored to the clinical situation. Schafer’s sign) indicates a probable retinal break.
Contusive trauma stresses the vitreoretinal inter- These pigmented cells gain access to the anterior
face and vitreous base, increasing the risk of vit- vitreous cavity through defects in the retina. The
reoretinal interface separation. Such a disruption presence of blood (vitreous hemorrhage) may
may lead to more sinister posterior segment indicate a disruption of the ciliary body, retina,
pathology. During the post-traumatic period, or retinal vasculature.
every patient should receive a complete ocular Indirect ophthalmoscopy should be performed
examination, including scleral depression with bilaterally in a systematic fashion. Examine the
ophthalmoscopic viewing of the ora serrata and optic disc, macula, vessels, and the complete
vitreous base. However, examination in the acute periphery. Special attention should be paid to
setting may be limited by the severity of injury, whitened areas of retina indicative of commotio
patient discomfort, and clarity of ocular media. retinae and the presence of subretinal hemor-
In lucid patients, best-corrected visual acuity rhage, which may herald a choroidal rupture. In
is measured with the Snellen chart. In an emer- the presence of intraocular hemorrhage or cor-
gency room setting, a Rosenbaum near card will neoscleral compromise, scleral depression should
suffice. Careful opening of the lids with Des- be deferred until structural stability is confi rmed.
marres lid retractors may be necessary if the However, scleral depression of the retinal periph-
patient is unable to open the eye due to lid edema ery to the vitreous base and ora serrata must be
or hemorrhage. Determination of pupillary light performed at some point in the post-traumatic
reaction and evaluation for a relative afferent period.
pupillary defect should be performed on every If patient discomfort or media opacities prevent
patient, regardless of consciousness. complete viewing of the ocular fundus and
Examination of the anterior segment prior to periphery, B-scan ultrasonography should be
further manipulation prevents iatrogenic injury. used to examine the posterior segment. Ultra-
Corneoscleral integrity and anterior chamber sound, in the hands of trained ophthalmic tech-
depth should be determined initially to rule out nicians, gives a significant degree of anatomic
105
Ocular trauma
Figure 8.2 A peripheral horseshoe retinal tear is seen B

on ultrasound in a patient with a traumatic vitreous
hemorrhage and a limited view of the posterior pole.
No retinal detachment is present.
detail. Occult retinal tears and/or detachments

can be detected without significant patient dis-
comfort (Figure 8.2). The presence of occult
tears or retinal detachments may necessitate
early surgical intervention. Ultrasound also
detects suprachoroidal hemorrhages or effusions,
posterior vitreous detachments, dislocated crys- Figure 8.3 (A) Photographic montage of central
talline or intraocular lenses, occult globe rup- (Berlin’s edema) and peripheral commotio retinae in a
16-year-old male who was struck with a fist. (B) Close-
tures, and intraocular foreign bodies.
up view of the retinal whitening seen in commotio
retinae. Note the marked contrast between involved
DIAGNOSIS AND TREATMENT OF and uninvolved retina.
SPECIFIC CLINICAL DIAGNOSES
Commotio retinae humans21 identified damaged photoreceptor

Commotio retinae, fi rst described in 1873, is the outer segments and retinal pigment epithelium.
most common retinal manifestation of contusive Intraretinal pigment migration and, in severe
ocular injury.18 Confluent geographic areas of cases, thinning of the outer retinal layers occurred
whitened retina most commonly appear in the following the acute phase. In vivo studies of
mid-periphery and less commonly in the macula acute commotio retinae by fundus reflection
(Figure 8.3). Commotio retinae involving the densitometry22 and optical coherence tomogra-
macula is also known as Berlin’s edema. It may phy23 also identified photoreceptor outer segment
occur following coup or countercoup injuries. and retinal pigment epithelium (RPE) damage.
Histopathologic studies in animals19,20 and in Fluorescein angiography performed 30 minutes
106
following contusive ocular trauma revealed stain- It is important to determine, if possible, the
ing of the RPE underlying the retinal whitening underlying cause of the vitreous hemorrhage,
but no leakage from retinal vessels. These results as treatment may vary. The most frequent
further suggest photoreceptor outer segment and causes of vitreous hemorrhage associated with
retinal pigment epithelium damage.24 trauma are posterior vitreous detachment, retinal
Acute vision loss may occur when commotio detachment, retinal tear, and pre-existing prolif-
retinae involves the macula, or it may be visually erative diabetic retinopathy.26–28 The presence of
asymptomatic if only the retinal periphery is vitreous hemorrhage in an infant or child should
involved. Vision typically improves as retinal alert the physician to the possibility of abuse.
whitening resolves. An experimental study of In this setting, photographic documentation
photoreceptor function reported recovery of and further investigation with a pediatrician is
normal function within 3 months. The prognosis vital.
is good for extrafoveal and mild trauma. However, Acute vitreous hemorrhage undergoes rapid
vision loss may be permanent if the fovea is clot formation and appears red with distinct
damaged. While 60% of patients in a prospective borders. Slowly, the blood begins to diffuse
study had complete recovery of vision within throughout the vitreous within the fi rst day to
weeks of injury, the remaining 40% were left week after the initial hemorrhage.29,30 In lique-
with macular damage and varying degrees of fied vitreous or a previously vitrectomized eye,
permanent vision loss. Long-term sequelae may blood clears from the vitreous cavity more rapidly
also include RPE changes and pigment migra- than in an eye with formed vitreous. 31 As red
tion. Such pigment migration in the retinal blood cells are phagocytosed and hemoglobin is
periphery may mimic the bone spicules of reti- broken down, the hemorrhage takes on a yellow-
nitis pigmentosa. Although there is no known brown hue as early as 10 days. The vitreous
treatment for commotio retinae, the frequency gel in an infant eye is more formed than in an
of concomitant ocular injury warrants close adult. Therefore, neonatal vitreous hemorrhages
observation and thorough examination. may sequester within Cloquet’s canal, remain
concentrated for long periods, and reabsorb
Traumatic vitreous hemorrhage slowly. 32
Common symptoms of vitreous hemorrhage If dense vitreous hemorrhage precludes ade-
include sudden, punctate, or web-like floaters quate ophthalmoscopic retinal viewing, ultra-
and decreased visual acuity. Sometimes patients sound provides an alternative examination.
will literally report seeing red. While the density Echography most effectively determines the
and location of the hemorrhage primarily deter- presence or absence of intraocular foreign
mine visual acuity, a small amount of blood can bodies, eyewall deformities, or retinal detach-
cause a significant decrease in vision. Thompson ments. Mild to moderate vitreous hemorrhage
and Stoessel reported that although 0.832 micro- appears as mobile opacities on B-scan and as
liters of diffuse vitreous blood caused no decrease low-amplitude spikes on A-scan, while marked
in vision, 10 microliters of vitreous blood can vitreous hemorrhage displays denser echoes on
decrease vision to hand motions or worse in a B-scan and higher amplitude spikes on A-scan.
phakic eye model. Furthermore, visual acuity If hemorrhage accumulates under the posterior
measured in light was worse than acuity mea- hyaloid, the increased reflectivity along the
sured in dark, owing to intraocular light scatter.25 hyaloid surface may mimic a retinal detachment.
107
Ocular trauma
However, positional shifting of the hemorrhage Vitreoretinal surgeons perform vitrectomy for
distinguishes it from the retina. 33 A-scan and B- traumatic vitreous hemorrhage only if the hem-
scan ultrasound examination of eyes with dense orrhage shows no sign of resolution. In an other-
vitreous hemorrhage often successfully identifies wise normal eye with normal serial ultrasounds,
retinal detachments, but echographic detection vitrectomy can be delayed depending on the
of retinal tears is challenging. 34 Among eyes with visual acuity in the fellow eye and the functional
dense vitreous hemorrhage, Rabinowitz reported status of the patient. Most surgeons will wait at
all retinal detachments (30 eyes) were identified least 2–3 weeks for a posterior vitreous detach-
correctly with an 18.9% false-positive rate, ment to develop and will intervene surgically
whereas only 44% of retinal tears were identi- only if the hemorrhage persists for more than
fied.8 In contrast, DiBernardo reported 10 of 11 2–3 months. 37
(91%) small retinal tears associated with vitre- If a retinal tear is identified and vitreous hem-
ous hemorrhage were diagnosed correctly by orrhage precludes laser demarcation, vitrectomy
ultrasound. 35 While ultrasonography remains is often performed within 2 weeks of presenta-
largely operator-dependent and has limitations tion, as progression to retinal detachment typi-
when ruling out small tears, it detects serious cally occurs within that period. In the setting of
posterior segment pathology that would other- traumatic vitreous hemorrhage, patients with a
wise remain hidden until hemorrhage dissolu- history of retinal detachment in the contralateral
tion or surgical exploration occurred. eye should be considered for earlier vitrectomy. 38
In a closed globe injury with vitreous hemor- In the presence of retinal detachment, early vit-
rhage but no retinal detachment or retinal break, rectomy should be performed, typically within
patients are observed to allow spontaneous clear- 1 week. Among a survey of vitreoretinal sur-
ance of the hemorrhage. 36 Bed rest and head geons, surgery for vitreous hemorrhage with
elevation are generally recommended to allow retinal tear was performed at a mean 1.7 weeks
gravitational settling of the hemorrhage. Re- and vitreous hemorrhage with retinal detach-
examination for hemorrhage resolution or retinal ment at 1 week.
detachment should be scheduled within 2 weeks Children in the amblyopic age range present a
of the initial evaluation. No topical medications therapeutic challenge. It is imperative to watch
have proven beneficial to speed the clearing of children with vitreous hemorrhage closely until
isolated vitreous hemorrhages. resolution or until the decision for surgery is
In eyes without a pre-existing vitreous detach- made. In infants, deprivation amblyopia may
ment, a posterior vitreous detachment com- occur within weeks of a dense vitreous hemor-
monly develops in the weeks following contusive rhage. 39 Mohney reported that an increase in
trauma. This independently increases the risk of axial length (averaging 3.45 mm more than the
subsequent retinal tear or detachment, making unaffected fellow eye) can occur within weeks
follow-up examinations important. If the view of vitreous hemorrhage onset.40 Such asymmet-
remains limited, the treating ophthalmologist ric axial lengths may cause anisometropia as
should perform serial ultrasound screening for great as 11 diopters. The pediatric patient’s age
posterior segment pathology. If vitreous hemor- and hemorrhage density guide the timing of
rhage remains for several weeks or if potential vitrectomy. Patients less than 1 year old
retinal pathology is detected, vitreoretinal con- develop myopic anisometropia more readily
sultation should be sought. than older patients.41 Typically, surgeons perform
108
vitrectomy for these patients within 3–4 weeks

of hemorrhage onset. In the postoperative period,
children require close follow-up for accompany-
ing injuries, anisometropia, and late traumatic
sequelae, such as cataract or angle recession
glaucoma. Furthermore, these patients must be
treated aggressively for amblyopia under the care
of a pediatric ophthalmologist. Despite appro-
priate surgical intervention to clear vitreous
hemorrhage, irreversible amblyopia may develop
in newborns.
Nonclearing vitreous hemorrhage may cause
secondary complications, such as glaucoma,
hemosiderosis, and proliferative vitreoretinopa-
thy. Secondary open angle glaucoma from vitre-
ous hemorrhage occurs due to breakdown of red Figure 8.4 Synchysis scintillans following vitreous
hemorrhage.
blood cells and may be classified into ghost cell,
hemolytic, or hemosiderotic glaucomas. Long-
standing vitreous hemorrhage may also cause pletely understood, surface traction at the vit-
retinal damage through chronic iron toxicity.42 reoretinal interface during equatorial expansion
Using radiolabeled 60Fe in rabbit eyes, Regnault of the globe and flattening of the posterior pole
reported 25% and 29% of iron was still present likely initiates hole formation.45 Vitreomacular
in ocular tissues 2 months after hemoglobin or traction in the setting of a delayed, trauma-
whole blood injection, respectively. 30 Breakdown induced posterior vitreous detachment may
of erythrocyte cell membranes can sometimes induce macular hole formation days to weeks
cause synchysis scintillans (also known as chol- following trauma.46 Reported causes of traumatic
esterolosis bulbi). This collection of colorful macular hole include:
cholesterol crystals may develop within the vit- 1. contusive ocular trauma47–49
reous cavity or anterior chamber but is rarely 2. electrical injury50,51
visually significant (Figure 8.4). Vitreous hemor- 3. Nd:YAG laser52,53
rhage may also stimulate fibrovascular pro- 4. thermal laser.54,55
liferation with subsequent tractional retinal Overall, trauma has been reported to cause
detachment; however, this more commonly nearly 10% of all full-thickness macular
occurs in eyes with penetrating injuries.43,44 holes.56,57
Acute traumatic macular holes are typically
Traumatic macular hole less than 1/2 disc diameter in size, although
The fovea is avascular and lacks structural chronic traumatic holes may grow larger.58 The
support from the inner retinal layers. Acute con- holes may be round or oval in shape. Vision typi-
tusive injury in an eye without a pre-existing cally remains 20/400 or better. Aside from a
posterior vitreous detachment may cause a full- history of ocular trauma, the more common
thickness macular hole at the time of impact. idiopathic macular holes may be clinically indis-
Although the mechanism of formation is incom- tinguishable from traumatic macular holes.
109
Ocular trauma
Traumatic macular holes have a variable natural improved hole closure rates when compared
history. Spontaneous closure of traumatic with observation alone. However, critics of
macular holes with improvement in visual acuity surgery performed in the early post-traumatic
is well documented.59–65 Small case series ranging period cite similar fi nal visual acuity outcomes
from 6 to 18 eyes report spontaneous closure in patients observed versus those repaired surgi-
rates of 10–67%. The overall incidence of spon- cally. While delaying surgery for a few months
taneous closure cannot be determined without to assess for spontaneous closure has been advo-
observation of a large number of patients. cated by some, others claim that early surgery
However, those eyes that had spontaneous offers the best chance for visual recovery.
closure shared some clinical features: small hole Appropriate referral to a vitreoretinal special-
size (0.1–0.2 disc diameters), no posterior vitre- ist for defi nitive management is indicated. Repair
ous detachment, and no cuff of subretinal fluid. of traumatic macular holes includes pars plana
Spontaneous closure occurred within 1 month vitrectomy, posterior hyaloid dissection, fluid-
in 35% and within 9 months in all reported gas exchange, and long-acting intraocular gas
cases. Final visual acuity was 20/40 or better in tamponade. Anatomic closure rates following
55% and 20/100 or better in 70%. vitrectomy and gas tamponade range from 93%
Although many traumatic macular holes may to 100%. Final visual acuity improved to 20/50
close spontaneously, surgical intervention offers or better in 35–79%.66,67
CASE EXAMPLES
Case report: traumatic macular hole and retinal tear (Figure 8.5)
A 16-year-old female was the victim of a drive-by (white arrow, B) with associated hemorrhage. The
paintball shooting. The paintball struck the left lower patient underwent a scleral buckle procedure, pars
eyelid (A) causing immediate pain and decreased plana vitrectomy with posterior hyaloid dissection
vision. Initial visual acuity was 20/200 in the involved and peeling of the internal limiting membrane,
left eye. The left pupil was enlarged and sluggish, endolaser, and injection of C3F8 gas for intraocular
but no relative afferent pupillary defect was present. tamponade. (C) Before and after ocular coherence
Anterior segment examination revealed conjunctival tomography scans reveal resolution of the macular
injection, a small hyphema, and mild traumatic hole. (D) Despite an excellent anatomic result, visual
mydriasis. Posterior segment examination revealed a acuity remained 20/200.
small macular hole and a large inferior retinal tear
110
Case report: traumatic macular hole and retinal tear (cont’d)
A B
C D
Choroidal rupture Choroidal ruptures are classified based on their

As described by von Graefe in 1854, a choroidal location. Direct ruptures occur at or near the site
rupture is a traumatic break in the retinal of contusive injury and are located anteriorly,
pigment epithelium (RPE), Bruch’s membrane, frequently parallel to the ora serrata.71 Indirect
and the underlying choroid.68 They are classi- ruptures are much more common and occur
cally cresent-shaped with tapered ends concen- distant from the impact site, typically within the
tric to the optic nerve (Figure 8.6). The acute posterior pole. They are classically found in a
lesions appear yellow to orange in color, but are concentric pattern adjacent to the optic nerve,
typically not visible owing to overlying subreti- usually temporal to the disc.72,73 The proposed
nal hemorrhage.69 With time, connective tissue mechanism of indirect choroidal rupture includes
grows over the break and pigmentation occurs rapid globe deformation with the optic nerve
along the borders.70 serving as a tethered stabilization point around
111
Ocular trauma
Epiretinal membranes develop from glial prolif-

eration through small, trauma-induced breaks in
the internal limiting membrane.83 An epiretinal
membrane appears as a transparent sheen or as
an opaque white tissue overlying the retina. As
the membrane contracts, there may be dragging
and straightening of vessels with or without
retinal striae.
Choroidal neovascularization may have a role
in the healing of choroidal ruptures, although
the neovascular membranes often spontaneously
regress. Clinically, choroidal neovascular mem-
branes (CNVM) appear as grayish-green sub-
retinal lesions often associated with subretinal
Figure 8.6 Multifocal choroidal rupture involving the hemorrhage and fluid. Choroidal neovasculariza-
fovea of a young child. tion occurs in 15–30% of traumatic choroidal
ruptures as early as 1 month after injury. There
may be an underestimate of the actual incidence
which the choroidal rupture develops. Multiple of CNVM since asymptomatic extrafoveal or
rupture sites have been reported in 19–37% of peripapillary membranes escape presentation to
all eyes with ruptures, and 50–66% of ruptures an ophthalmologist. Secretan and colleagues
involve the macula. As with most traumatic inju- reported that choroidal neovascularization was
ries, males are more commonly affected. more likely to develop from ruptures closer to
Immediate vision loss occurs with direct the foveal center and with greater rupture length.
involvement of the macula or associated serous The majority of eyes (81.2%) in their study
detachment, retinal edema, or hemorrhage.74–76 developed a neovascular membrane within 1
In most cases, visual acuity recovers as the fluid year of injury.73
or hemorrhage resolves. While patients may Fluorescein angiography confi rms the presence
complain of a scotoma, the site of choroidal of a presumed CNVM. Choroidal ruptures
rupture does not always correlate with visual appear as window defects without appreciable
field defects.77 Furthermore, the size of the field leakage. If choroidal neovascularization is
defect may appear larger than clinical examina- present, the lesion will typically hyperfluoresce
tion would predict, suggesting overlying retinal early and leak late. The presence of blood may
damage is more extensive than the rupture site interfere with clinical examination or fluorescein
itself.78 Rupture location often determines fi nal angiography, obscuring the presence of choroidal
visual outcome with foveal involvement typically neovascularization. Indocyanine green (ICG)
causing permanent visual acuity loss. Neverthe- angiography is a useful alternative for identifying
less, some patients with subfoveal rupture retain and characterizing choroidal ruptures and asso-
20/20 vision. ciated choroidal neovascularization that may be
Epiretinal membrane formation,79 serous obscured by overlying hemorrhage.84–86
retinal elevation,80 or choroidal neovasculari- No treatment exists for a traumatic choroidal
zation81,82 may cause delayed-onset vision loss. rupture. Regular funduscopic examination
112
should be performed every 6 months for the fi rst the macula, membranes nasal to the disc are
2 years following the injury to detect the devel- often observed. Occasionally, spontaneous invo-
opment of choroidal neovascularization. Careful lution occurs.
attention for the development of CNVM is war- Visual prognosis depends on the rupture size,
ranted for ruptures longer than 4000 μm or location and secondary complications (particu-
within 1500 μm of the foveal center. For these larly CNVM). Hemorrhage or edema may affect
larger ruptures, long-term follow-up is recom- vision in the acute setting, but presenting visual
mended since choroidal neovascularization has acuity is not a prognostic factor. Visual acuity
been reported to occur up to 37 years following typically recovers in eyes with non-foveal rup-
the injury.87 The treating ophthalmologist should tures. Greater rupture length portends a poor
instruct patients experiencing a decline in vision visual outcome, owing to the risk of choroidal
or metamorphopsia to return immediately for a neovascularization. Close proximity to the fovea
dilated examination. also heralds poor visual acuity from damaged
Therapeutic options for CNVM include macular photoreceptors. Furthermore, multiple
observation, photocoagulation,87 photodynamic rupture sites indicate severe ocular trauma, likely
therapy,89,90 or submacular surgical removal. The with concomitant ocular injuries. Associated
use of drugs which target vascular endothelial injuries such as macular hole, pigment epithelial
growth factor (VEGF) is a new modality that is atrophy, commotio retinae, or optic atrophy may
being investigated. Since they are distant from adversely affect visual recovery.
CASE EXAMPLES
Case report: choroidal rupture with CNVM (Figure 8.7)

A 32-year-old male presented to the emergency A
room with complaints of distorted vision in his right
eye. Several years prior to this, he had been struck in
the right eye with a fist and had a moderate decline
in visual acuity. However, he had noted a distinct
change in the quality of the vision over the previous
2–3 days. Examination revealed a visual acuity of
20/100 with a normal intraocular pressure. Slit lamp
examination was unremarkable. Dilated fundus
examination revealed a choroidal rupture that began
approximately a disc area temporal and slightly
superior to the fovea and extended inferonasally,
ending just inferior to the fovea. Pigmentary alter-
113
Ocular trauma
Case report: choroidal rupture with CNVM (cont’d)

ations and an epiretinal membrane were present the CNVM and staining of the nasal macula (C).
nasal to the fovea. Of note, the superotemporal The diagnosis of choroidal rupture-associated
portion of the choroidal rupture was associated with CNVM was made. The patient was given multiple
an elevated subretinal lesion surrounded by a cuff of therapeutic options. Given the proximity of the
subretinal fluid (A), consistent with a choroidal lesion to the fovea and the patient’s desire to
neovascular membrane (CNVM). Fluorescein angio- avoid laser treatments, an intravitreal injection of
graphy (FA) was obtained. Early frames of the FA an anti-VEGF agent was given. On follow-up, the
revealed early hyperfluorescence of the choroidal CNVM resolved completely with resolution of
rupture and CNVM as well as mottled hyperfluo- the patient’s metamorphopsia. The visual acuity
rescence in the area of pigmentary alteration in the remained unchanged.
nasal macula (B). Late frames reveal leakage from
B C
Suprachoroidal hemorrhage rhagic choroidals most commonly occur with

Traumatic suprachoroidal hemorrhage, or hem- penetrating ocular injuries95,96 and should raise
orrhagic choroidal detachment, occurs when the suspicion for an open globe when encoun-
blood accumulates within the potential space tered. Less commonly, sudden decompression of
between the choroid and the sclera. This poten- the globe during contusive trauma can create a
tial space extends from the scleral spur anteri- similar picture.97
orly to the optic nerve posteriorly. The choroid Traumatic suprachoroidal hemorrhage may
is anchored at the vortex veins, leading to the present with a shallow or flat anterior chamber,
characteristic dome-shaped appearance of cho- with or without expulsion of intraocular con-
roidal detachments. Hemorrhage occurs follow- tents. Pain and elevated intraocular pressure
ing rupture of the long or short posterior ciliary often result if the globe remains intact. Fundo-
arteries91–93 or ciliary body vessels. 94 Hemor- scopic examination reveals dark, dome-shaped
114
elevations of the retina and choroid, causing a A

loss of the red reflex. A limited suprachoroidal
hemorrhage often appears as a wedge-shaped
elevation with the apex aimed at the posterior
pole. If the choroidal detachment remains local-
ized to the periphery, visual acuity may be unaf-
fected. However, choroidal detachments within
the posterior pole cause profound loss of visual
acuity, possibly to no light perception. 98
Ultrasound evaluates with excellent detail the
extent and characteristics of suprachoroidal
fluid, as well as the overlying retina and vitreous.
Hemorrhagic choroidal detachments on B-scan B
ultrasound appear as non-mobile, flat or dome-
shaped echo-dense opacities within the supra-
choroidal space (Figure 8.8).99 Echography also
determines clot lysis and liquefaction, which
helps determine the timing of surgery to remove
the liquefied clot. Initially A-scan echography
reveals a highly reflective collection of clotted
blood within the suprachoroidal space. With
time, A-scan reflectivity decreases as the clot
breaks down, and B-scan reveals more echo-
lucent and mobile echoes beneath the choroid. Figure 8.8 (A and B) Suprachoroidal hemorrhage
Average time to clot liquefaction is 10–14 detected on B-scan ultrasonography following severe
contusive ocular trauma.
days.100,101
Suprachoroidal hemorrhage associated with a
closed globe injury (or following repair of an to a poor visual prognosis include 360 degrees of
open globe injury) may be observed, especially choroidal hemorrhage, vitreous or retinal wound
if the hemorrhage does not involve the posterior incarceration, retinal detachment, and apposed
pole. Some suprachoroidal hemorrhages resolve retinal surfaces for more than 14 days. In open
without surgical intervention; however, late globe injuries, retinal detachment or additional
complications such as retinal detachment can trauma-related injuries often complicate the
occur.102,103 Most surgeons recommend waiting postoperative course and contribute to poor
until there is adequate clot lysis, as determined visual outcomes. Properly timed surgical inter-
by echography, prior to surgical intervention. vention should be tailored to the individual
When indicated, drainage of suprachoroidal patient under the guise of a vitreoretinal
hemorrhage is usually performed between 7 and specialist.
14 days post injury.104,105
Traumatic suprachoroidal hemorrhage typi- Sclopetaria
cally has a poor visual outcome regardless of Sclopetaria, or traumatic chorioretinal rupture,
early surgical intervention. Factors contributing is a rare entity. It was fi rst described in the
115
Ocular trauma
German literature as a full-thickness rupture of

the retina and choroid following orbital injury
with a high-velocity missle.106,107 The missile typ-
ically passes adjacent to the globe, penetrating
the orbit at high velocity without violating the
eyewall.108 Sclopetaria has been reported follow-
ing non-penetrating gunshot wounds,109–112 BB
injuries,113–115 or other projectile injuries.116–118
Damage most commonly occurs along the path
of the projectile as it enters the orbit. Rapid
deformation of the globe creates tension on ocular
tissues. The traumatic stress induced by the high-
velocity projectile exceeds the tensile strength of Figure 8.9 Sclopetaria is seen in a young patient who
the retina and choroid, thereby causing retrac- suffered a gunshot wound that passed through the
orbit without direct contact with the globe. Severe
tion of these two tissues together, while the
fibrosis and loss of retinochoroidal architecture follows
underlying sclera remains intact. the course of the projectile through the orbit.
The extent of the chorioretinal damage depends
on the size, velocity, and proximity of the pro-
jectile to the globe. Fibrous proliferation during coherence tomography can be helpful in differ-
the healing process anchors the retinochoroidal entiating between chorioretinal edema and a
margin to the underlying sclera. Surrounding true retinal detachment. Damage to the retinal
pigmentation occurs within days to weeks. After circulation outside the ruptured areas causes
associated hemorrhage or edema clears, the visual field defects distant to the areas of scar-
affected area appears scarred and atrophic with ring. Visual field testing often shows larger
serrated, pigmented margins. The full-thickness defects than would be predicted by sclopetaria
chorioretinal break may reveal underlying bare size alone.
sclera or secondary fibrotic tissue (Figure 8.9). Patients may experience acute loss of vision
Additionally, preretinal gliosis may occur at sites depending on the location of the injury. Final
distant to the chorioretinal rupture. Despite the visual acuity of 20/20 has been reported in
intensity of the injury, the overlying posterior several cases. If the macula is involved, profound
hyaloid face may not be disrupted. In fact, the and permanent visual loss typically occurs. If the
vitreous often strongly adheres to the rupture macula remains uninvolved, related traumatic
edges. Indirect trauma, including posterior cho- injuries primarily cause visual loss.
roidal ruptures and macular damage, commonly Since the high-velocity nature of the injury
occurs simultaneously with sclopetaria. Con- seals the retina and choroid to the underlying
comitant retinal tears may also be present, sclera, surgical intervention is rarely required.
making a complete peripheral retinal exam Retinal detachment uncommonly follows sclop-
necessary. etaria, making prophylactic cryotherapy, laser
Choroidal and retinal hemorrhage is often photocoagulation, or scleral buckling unneces-
present initially. Thickened, edematous retinal sary. Typically, treatment consists of observa-
margins may give the impression of a retinal tional management with continued long-term
detachment or tear. Ultrasonography or optical follow-up to screen for future post-traumatic
116
complications such as angle recession glaucoma, Retinal dialysis

vitreous hemorrhage, or retinal detachment. Pars plan Ora serrata
Traumatic retinal detachment

Traumatic retinal detachment is the fi nal
common pathway for the remaining clinical
entities described below. Once the clinician
diagnoses a retinal detachment, the patient Vitreous base
should be referred to a vitreoretinal specialist so insertion
that appropriate interventions can be performed.
Since patients with traumatic retinal detach-
ments frequently have concomitant ocular injury,
thorough examination and careful surgical plan-
ning yield the best chance for optimum recovery.
The clinical behavior and treatment strategies
Retina
for traumatic detachments often will vary
depending on the underlying cause.
Figure 8.10 An intact vitreous base associated with a
Retinal dialysis retinal dialysis allows little fluid to enter the subretinal
Retinal dialysis is a disinsertion of the retina space and inhibits proliferative vitreoretinopathy,
from the nonpigmented pars plana epithelium at leading to a slowly progressive retinal detachment or
the ora serrata. The disinserted retina remains even spontaneous healing.
attached to the vitreous base (Figure 8.10). Dial-
ysis has been reported to cause 7% of rhegmato- thereby inducing a tractional force that weakens
genous retinal detachments. Trauma, myopia, the retina in this region.126 Furthermore, the ora
and congenital weakness of the peripheral retina serrata is the thinnest portion of the retina. Tem-
may all contribute to the development of a dialy- porally, there is little protection from the nasal
sis. Myopia was present in 11% of patients in two bridge or bony orbital rim. Relatively weak retina
different large series,119,120 and a heritable weak- with relatively less bony protection may predis-
ness of the peripheral retina has been suggested pose to inferotemporal dialysis, even with minor
as an independent cause.121,122 However, clinical trauma as an initiating factor. Between 22% and
evidence has shown trauma to be the primary 68% of unilateral inferotemporal dialyses have
cause in the majority of cases.123–125 In a series of been associated with a defi nite history of prior
586 detachments, a history of trauma was trauma. The most common location of trauma-
reported in 87% of superonasal dialyses and in related dialyses is the superonasal quadrant.127,128
61% of inferotemporal dialyses. This underscores the importance of countercoup
The most common location for dialyses of all injuries since the inciting injury typically is
origins is the inferotemporal quadrant. Embryo- directed at the inferotemporal quadrant, the
logic studies have shown that the inferotemporal least protected area of the eye.
quadrant contains the weakest peripheral retina Similar to detachments associated with pars
because the temporal pars plana grows more plana tears, detachments associated with retinal
rapidly than the temporal peripheral retina, dialysis typically have few symptoms. They may
117
Ocular trauma
remain undiagnosed for long periods of time and Pars plan Ora serrata
may heal spontaneously. In one series of dialysis-
related detachments 37% of detachments pre-
sented more than a year following trauma. The
detachments are typically shallow and smooth,
since the intact vitreous tamponades the break
Vitreous base
and prevents large amounts of vitreous fluid insertion
from entering the subretinal space. Signs of
chronicity include: retinal macrocysts, atrophic
retina that resembles a retinoschisis, and pro-
gressive pigmented demarcation lines beneath
the retina.129
Giant retinal tears Retina

A giant retinal tear extends for at least 90 degrees,
or 3 clock hours, in circumferential extent. Giant
retinal tears most commonly occur with no ante- Figure 8.11 Horseshoe tears occur along the vitreous
cedent trauma and account for approximately base in the presence of a posterior vitreous
25% of all tears in several published series. Many detachment. Giant retinal tears occur when the tear
extends along the posterior edge of the vitreous base
non-traumatic giant tears are associated with
(hatched line) for >3 clock hours.
myopia. Giant tears have been reported in 16%
of traumatic retinal detachments, of which the
majority of eyes were emmetropic.130–133 Based usually a month or less. By comparison, giant
on this epidemiologic information, there appear retinal tears related to penetrating ocular trauma
to be two primary mechanisms in the formation often present with detachment more than a
of giant tears: contusive ocular trauma to an month later, owing to delayed posterior vitreous
otherwise normal eye and spontaneous giant tear detachment or proliferative vitreoretinopathy.
formation in the myopic eye. In reality, a spec- Almost all giant tears are associated with a
trum of scenarios produce giant tears, with posterior vitreous detachment. The collapsing
varying degrees of predisposing myopia com- vitreous creates the tear and remains attached
bined with a varying severity of precipitating only to the anterior leaflet of retina, thus
trauma. Demographically, trauma-induced giant allowing free mobility of the posterior flap
retinal tears occur most commonly in young (Figure 8.11). This mobile posterior flap of retina
males. In a study of 586 traumatic and non- facilitates the entrance of liquefied vitreous into
traumatic retinal detachments, a history of the subretinal space and can lead to rapidly pro-
trauma was elucidated in 67% of patients with gressing detachments, particularly if the tear is
giant tears. superior in location (Figure 8.12).
Giant retinal tears, like other traumatic retinal
breaks related to contusive trauma, are typically Horseshoe tears
located in the inferotemporal or superonasal Areas of strong vitreoretinal adhesion cause
quadrants. The duration of time from contusive retinal breaks during traumatic or spontaneous
eye trauma to diagnosis of retinal detachment is posterior vitreous detachment. These retinal
118
vitreous traction, allowing fluid to continually

enter the subretinal space. Unlike retinal dialy-
ses or pars plana tears but similar to giant retinal
tears, detachments associated with horseshoe
tears tend to progress rapidly and symptomati-
cally to bullous detachments.
Necrotic retinal breaks

Whereas retinal dialyses and pars plana tears
occur anteriorly, necrotic retinal breaks are found
posterior to the ora serrata, oftentimes in the
equatorial region. In a series of 445 eyes with
fundus changes caused by contusive ocular
trauma, approximately 1/3 of retinal tears
Figure 8.12 A posterior vitreous detachment exerts detected were located near the equator.134
persistent traction on the posterior lip of torn retina, Direct contusive trauma may cause retinal
frequently leading to rapid influx of fluid into the necrosis and ischemia at the impact site. In one
subretinal space and a rapidly developing retinal
study, irregular necrotic retinal breaks were
detachment. Modified from Ryan SJ. Retina, 4th ed.
St Louis: Mosby, 2006. found to be the cause of 22% of trauma-related
retinal detachments over an 8-year period.135
Direct contusive damage to the retina, retinal
breaks typically take the shape of a horseshoe. vascular damage, and retinal capillary necrosis
Detachments related to horseshoe tears have contribute to the weakened retina at the impact
been reported to account for 11% of traumatic site.136 Similar injury following countercoup
retinal detachments and 45% of spontaneous trauma has also been reported.137 Such damage
detachments. Furthermore, a history of trauma may result in the formation of irregularly shaped
was present in 5% and objective evidence of retinal breaks. The most common location of
trauma was found in 20% of detachments associ- such breaks is the inferotemporal quadrant, due
ated with horseshoe tears. As would be expected, to the more exposed position of the globe and
patients with trauma-related horseshoe detach- the natural supraduction of the eye with lid
ments are younger than those with non-traumatic closure (Bell’s phenomenon). Detachments asso-
detachments. However, assigning a traumatic ciated with necrotic retinal breaks tend to form
etiology to these cases can be difficult. quickly, often within 24 hours.
When vitreous syneresis leads to a posterior
vitreous detachment, horseshoe tears normally Vitreous base avulsion
occur at sites of vitreoretinal adhesion. A similar Contusive ocular injury may avulse the vitreous
mechanism occurs in traumatic horseshoe tear base from its fi rm adhesion straddling the ora
development. Globe deformation and torsion serrata. In fact, vitreous base avulsion is consid-
lead to posterior vitreous detachment, and a tear ered pathognomonic for contusive ocular trauma.
can develop at the site of fi rm vitreoretinal adhe- Vitreous base avulsion has been reported in
sion. A flap of retina is held open by residual 25.9% of patients with traumatic retinal detach-
119
Ocular trauma
ment. Vitreous base avulsions have been reported nations are important as the vitreous separation
to occur in roughly half of patients with retinal evolves over days to weeks.
detachments secondary to squash ball injuries.138
The trauma associated with vitreous base avul- Pars plana tears
sion is often presumed severe considering the The non-pigmented pars plana epithelium is the
vitreoretinal adhesions are often strongest at the anterior extension of the neurosensory retina.
vitreous base. Because of this inherently strong Pars plana tears result almost exclusively from
vitreoretinal adhesion, avulsion without con- closed globe contusion. The contusive forces place
comitant pars plana tears, retinal dialyses, or traction on the anterior border of the vitreous
retinal tears is uncommon. Vitreous base avul- base, resulting in tear formation. Penetrating
sions appear as a stripe of translucent vitreous ocular injury, posterior segment surgery, and
overlying the peripheral retina or ora serrata, atopy are the only other documented causes.139–141
yielding a ‘bucket handle’ appearance. This con- Interestingly, the retinal tears and detachments
dition may be asymptomatic and requires no associated with atopic dermatitis may be con-
treatment if found in isolation. However, the sidered traumatic in origin, given the clinical
presence of this fi nding should alert the clinician nature of the tears and the propensity for vigorous
to perform a careful examination of the pars ocular rubbing seen in this population.
plana, ora serrata, and retinal periphery when Pars plana tears are uncommon, seven times
the eye becomes stable enough for scleral depres- less commonly diagnosed than retinal dialysis.
sion, as the incidence of retinal tears and dialyses However, it is likely that pars plana tears are
is very high. underdiagnosed since they are usually not associ-
ated with retinal detachment and can only be
Traumatic posterior vitreous detachment seen with anterior scleral depression. The pres-
Traumatic posterior vitreous detachment (PVD) entation and clinical course of retinal detach-
alone or in combination with vitreous hemor- ments associated with pars plana epithelium
rhage is frequently encountered following closed tears are similar to those caused by retinal dialy-
globe eye injury. Although neither condition sis. The detachments are shallow with smooth
alone causes permanent loss of function, their surfaces. They progress slowly over several
presence often heralds more sinister pathology, months and are generally asymptomatic until
particularly of the peripheral retina. Vitreoreti- they involve the macula.142 The typical shallow,
nal adhesions are much greater in young patients. slowly progressive nature of these detachments
Since trauma occurs much more frequently in is due to the absence of a posterior vitreous
young patients (particularly males), the likeli- detachment and the anterior tear location. The
hood of retinal tears in the setting of a traumatic posterior vitreous base remains attached, provid-
PVD is very high. Examination of the anterior ing a tamponade that limits access of liquefied
retina and pars plana is vital. If it cannot be vitreous to the subretinal space.
performed in the acute setting owing to con-
comitant ocular injury, patient discomfort, or a Treatment
poor view due to hemorrhage, ultrasonography Traumatic breaks that lead to rapid retinal
is an excellent tool to determine if any peripheral detachment include necrotic retinal breaks,
tears or detachments are present. Serial exami- horseshoe tears, and giant retinal tears. At times,
120
the vitreous may remain formed in eyes with Visual acuity outcomes are variable. One large
traumatic tears, and chorioretinal adhesions may series reported that nearly 65% had a fi nal visual
form that lead to spontaneous hole closure. Such acuity of 20/200 or better with a range of 20/20
eyes should be monitored closely for progression to no light perception. Concomitant macular
to detachment. Prophylactic laser retinopexy or pathology may limit visual acuity following
trans-scleral cryopexy should be considered in repair, particularly epiretinal membranes and
all patients with traumatic peripheral retinal macular edema.
breaks in the absence of significant subretinal Anterior traumatic pathology, such as pars
fluid. Once a detachment forms, surgical inter- plana tears and retinal dialyses, may lead to a
vention is required. As in repair of non- slowly developing, asymptomatic retinal detach-
traumatic detachments, the overall goal of ment. Such breaks should be treated with
surgery is to close all retinal breaks and to relieve cryopexy or laser retinopexy in the acute post-
all vitreoretinal traction. Retinal reattachment traumatic period if no significant subretinal fluid
may be achieved through pneumatic retinopexy, is present. If asymptomatic subretinal fluid is
scleral buckling, and/or pars plana vitrectomy. detected months to years after trauma, assess for
The specific clinical situation and surgeon pref- stable chronicity of the break and subretinal
erence determine the method of repair. fluid. Signs of chronic subretinal fluid include
Giant retinal tears rarely present without con- retinal atrophy, retinal macrocysts, absence of
current retinal detachment owing to the mobile rugae, and the presence of demarcation lines. If
posterior retinal flap that allows free entry of a demarcation line has developed, the retinal
fluid into the subretinal space. Moreover, the break and subretinal fluid may heal spontane-
retina may fold upon itself preoperatively or ously, requiring only close observation. In the
intraoperatively. These tears often require presence of significant subretinal fluid without
advanced vitreoretinal techniques such as demarcation, surgical intervention is indicated.
perfluorocarbon stabilization, lensectomy, and Detachments associated with pars plana tears
silicone oil tamponade. Despite advances in or retinal dialyses may be repaired with good
vitreoretinal surgery, redetachment rates follow- results by scleral buckling with trans-scleral
ing repair may exceed 10% (Figure 8.13).143 cryotherapy or by scleral buckling with pars
plana vitrectomy, fluid–air exchange, internal
drainage of subretinal fluid, and endolaser
photocoagulation.
CONCLUSION
Posterior segment manifestations of contusive

ocular trauma may cause severe vision loss, even
years after the trauma. Detection of all injuries
by thorough examination followed by prompt
treatment offers the best chance to maintain
Figure 8.13 A complex, recurrent trauma-related optimum vision. Furthermore, ocular contusion
retinal detachment is visible through the dilated pupil. with enough force to cause posterior segment
121
Ocular trauma
damage often causes multiple ocular injuries. 6. Vitreous hemorrhage is of particular concern
Although each posterior segment injury was dis- in young children since amblyopia and pro-
cussed individually, it is important for the clini- gressive myopia may develop rapidly.
cian to maintain a high level of suspicion for 7. Choroidal ruptures require serial monitor-
coexisting systemic, orbital, anterior segment, ing for the appearance of choroidal neovas-
and posterior segment injuries. cular membranes.
Manifestations of posterior segment trauma 8. Suprachoroidal hemorrhage indicates severe
without retinal breaks (vitreous base avulsion ocular trauma and portends a poor visual
and commotio retinae) may be carefully observed prognosis.
with short interval serial examinations in the post- 9. Sclopetaria is a rare but characteristic mani-
traumatic period. Examinations should include festation of high-velocity missile injury.
scleral depression to the ora serrata once the eye 10. The type of peripheral break in the retina or
is stable enough to sustain scleral indentation or pars plana has significant bearing on the
serial ultrasounds if media opacity or patient future behavior of retinal detachments and
discomfort precludes ophthalmoscopic examina- their subsequent repair.
tion. Once the diagnosis of a retinal break or 11. Retinal detachment is the fi nal common
detachment is made, vitreoretinal consultation is pathway for disturbances of the vitreoretinal
indicated. interface.
SUMMARY REFERENCES
1. Contusive ocular injury frequently involves 1. Goffstein R, Burton TC. Differentiating traumatic from
the posterior segment and has frequent nontraumatic retinal detachment. Ophthalmology
1982;89:361–368.
vision-threatening sequelae.
2. Dumas JJ. Retinal detachment following contusion of the
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126
9
eyelid lacerations
Kambiz K. Parsa, Wendy W. Lee
INTRODUCTION a larger tarsal plate, and maintains its position

primarily with the levator aponeurosis. The
The approach to any patient with trauma is uni- lower eyelid is smaller, is supported by a smaller
versal. The patient must be systematically evalu- tarsal plate, and maintains its position primarily
ated and life-threatening injuries, if present, with the lower eyelid retractors. Of particular
must be addressed and prioritized before evalu- interest is the lacrimal drainage system (Figure
ation of the eye and ocular adnexa begins. In this 9.4C), a system whose structural integrity is
chapter we will discuss the specifics of evaluat- paramount when evaluating and repairing eyelid
ing and treating a patient with an eyelid lacera- lacerations.
tion. Particular emphasis will be given to history
taking, physical examination, and surgical repair EVALUATION
of the most common types of eyelid lacerations.
More extensive eyelid and orbital injuries are Initial evaluation of the patient begins with a
beyond the scope of this text and require con- comprehensive history. Spending focused time
sultation with an oculoplastic specialist. on the history will help guide the physical exam-
Depending on the mechanism of injury, the ination. At times it may be difficult to obtain a
eyelids may display multiple injury types. These reliable history from the patient. Patients who
include: are under the influence of recreational drugs may
1. Contusion: superficial impact injury associ- not be good historians. Many patients with
ated with ecchymoses and soft tissue swelling extensive injuries may be unresponsive or even
(Figure 9.1) intubated. Children might attempt to conceal
2. Abrasion: scraping, usually an epithelial loss the details of injury for fear of parental punish-
3. Avulsion: tearing of tissue (Figure 9.2) ment. If attempts to obtain a reliable history
4. Puncture: passage of a sharp object through from the patient are unsuccessful, try to locate
tissue planes an eyewitness or family member who may be
5. Laceration: cut tissue, typically caused by a able to provide further detail.
sharp object (Figure 9.3). Focus should be placed on the timing, mecha-
The key to any good surgical outcome is a com- nism and location of injury. The time an injury
plete understanding of the regional anatomy. occurred needs to be carefully documented so
The eyelid is a unique structure that is anatomi- the physician can decide if adequate time has
cally divided into two layers, or lamellae (Figure passed for associated edema to subside or
9.4A). The anterior and posterior lamellae are improve. This in turn helps determine the timing
closed separately during full-thickness eyelid of repair.
laceration repair. The upper and lower eyelids Understanding the mechanism and location of
have important anatomical differences (Figure the trauma helps determine the extent and depth
9.4B). The upper eyelid is larger, is supported by of injury to the tissues and the likelihood of
127
Ocular trauma
Figure 9.1 Eyelid contusion, typical of assault-related Figure 9.3 Lacerations of the upper and lower eyelids
injuries. caused by injury with a shattered baseball bat.
by organic material (e.g. tree branch) may be

associated with a fungal infection or retained
particles. Animal bites, which should always be
reported to appropriate local authorities, are
often associated with deep puncture wounds
and have specific infection concerns. In all
patients with eyelid lacerations, maintain a high
index of suspicion for underlying globe trauma.
This is especially true with injuries caused by
sharp (e.g. pen, pencil, or knife) or high-velocity
objects (e.g. bungee cord).
The patient’s tetanus immunization history
should be obtained. Patients without previous
Figure 9.2 Upper eyelid avulsion. immunization should receive 250 units of human
tetanus immune globulin intramuscularly. If the
other associated injuries or retained foreign patient has not had a tetanus booster in the past
bodies. If the person was struck with an object, 10 years, administer intramuscular or subcuta-
several questions must be asked: neous tetanus toxoid (0.5 ml).1
1. Was the object blunt or sharp? A complete ocular exam is indicated in all
2. What was the constitution of the object trauma patients to assess potential damage to the
(organic vs. non-organic)? globe. After the eye has been fully evaluated (see
3. Was the object embedded in the eyelid and if Chapter 3), attention can be focused on the
so, was it removed? Was the object removed eyelids and ocular adnexa.
whole or in pieces? Most eyelid injuries can be examined at the slit
The answers to these questions further direct lamp without difficulty. However, the discom-
the examination and raise or lower the suspicion fort associated with extensive eyelid lacerations
of underlying globe injury. Eyelid injury caused usually makes complete inspection difficult
128
Closed globe injuries: eyelid lacerations
A
Posterior lamella Anterior lamella
Gray line
Meibomian gland orifice

C
Mucocutaneous Lacrimal gland
junction
Upper and lower
canaliculus
Lacrimal sac
Tarsus
Common
Meibomian canaliculus
glands
Upper and
lower punctum
Orbicularis
Nasolacrimal duct
B
Skin
Frontal sinus Frontalis muscle
Brow fat pad Figure 9.4 (A) The eyelid is
divided into an anterior lamella,
Levator muscle which includes the skin and the
Septum orbicularis oculi muscle, and the
Superior rectus muscle Preaponeurotic fat
posterior lamella which consists of
Levator aponeurosis
the tarsal plate and the
Müller’s muscle Orbicularis
conjunctiva. It is important to
realize that each segment has its
own blood supply and during
Tarsal plate reconstruction or laceration repair,
Meibomian glands each segment needs to be
realigned in its proper anatomic
position. (B) The tarsus, which is a
Tarsal plate semi-rigid structure, can be
thought of as the backbone of the
Inferior tarsal muscle eyelids. It extends vertically about
Inferior oblique muscle 10–12 mm on the upper eyelid
Septum
and 4 mm on the lower lid.
Inferior rectus muscle Lockwood’s
Superiorly it is attached to the
suspensory ligament
Capsulopalpebral fascia levator aponeurosis and Müller’s
Preaponeurotic fat
muscle. Inferiorly it is attached to
the lower eyelid retractors and the
inferior tarsal muscle. (C) Lacrimal
drainage system.
129
Ocular trauma
without use of local anesthesia. Furthermore, cating deeper orbital injury. Be suspicious of
complete inspection and cleansing of a wound is a levator aponeurosis laceration in this case.
typically not feasible without extensive mani- Horizontal upper eyelid lacerations associated
pulation. The authors prefer to anesthetize with acute ptosis may also indicate damage to
these wounds with a local injection of 2% the levator aponeurosis. However, assessing
lidocaine with epinephrine when the wound the level of ptosis may be difficult due to
must be manipulated or irrigated. Not only does severe periorbital swelling. Traumatic ptosis
this relieve pain, but it provides improved can occur without a laceration to the levator
hemostasis. muscle or aponeurosis.
• If the patient is conscious and responsive,
Inspection tips attempt to assess levator function by asking
• Anesthetize and cleanse the wound appro- the patient to look up. Horizontal lacerations
priately to allow for a more comfortable and of the levator aponeurosis often need repair,
complete examination. preferably by an oculoplastic specialist.
• Gently pull apart the wound, as fibrin may • Evaluate the degree of eyelid edema and
be holding the wound together and give the determine if wound edges can be reapproxi-
false impression that a laceration is less mated without tension. Wound tension can
extensive. lead to dehiscence and scarring.
• Inspect for foreign bodies. Retained orbital foreign bodies are a significant
• Inspect the eyelid margin. Evert the eyelid to concern as they can cause a severe inflammatory
look for posterior tarsal lacerations that may reaction or infection. If the possibility of a
not be associated with anterior lamellar foreign body exists, imaging is often employed
lacerations. to identify and localize the foreign material.
• Inspect the medial canthus carefully to look Computed tomography (CT) may confi rm or
for canalicular injuries. If you suspect a cana- reveal retained foreign bodies as well as detect
licular injury, carefully use a 00 Bowman retrobulbar hemorrhage, a violated globe or
probe inserted through both the upper and orbital fractures. If the possibility of a retained
lower punctum individually. If any portion of metallic foreign body can be eliminated by
the probe is exposed, a canalicular laceration history, examination, or plain radiographs, orbital
is confi rmed. Take care not to create a false magnetic resonance imaging (MRI) has higher
passage. resolution and can sometimes detect non-
• When the lacrimal system is injured, suspect metallic foreign bodies (e.g. organic material)
medial canthal tendon injuries. The lacrimal more readily than CT.
sac lies between the anterior and posterior
limbs of the medial canthal tendon. Look for EYELID LACERATIONS: GENERAL
lateral displacement of the medial canthal CONSIDERATIONS
angle. If suspicious, consult an oculoplastic
specialist. Once an eyelid laceration is identified, a surgical
• What may appear to be a simple anterior strategy is formulated. If periorbital swelling
lamellar laceration may extend into the deep precludes immediate closure, repair can be
layers. Look for orbital fat in the wound as a delayed several days if necessary. Waiting in such
sign that the septum has been violated, indi- a case is beneficial because edema may create
130
undue tension against the newly approximated • Anesthetize the tissues prior to cleansing and
wound and may distort the anatomy making inspecting as outlined previously.
optimal closure of the proper layers difficult. • Sterilize the surgical field with povidone
Postponing closure of an eyelid laceration is pos- iodine or an appropriate alternative if the
sible because of the extensive vascularity in these patient has an allergy to topical iodine.
tissues, a unique characteristic of the eyelid and • Isolate the wound with sterile drapes.
facial soft tissue. • Inspect for foreign bodies and irrigate copiously.
Ice packs are applied to the wound to decrease • Pull lacerated tissues apart during inspection,
swelling. An antibiotic ointment is used fre- as fibrin tends to hold lacerated edges together,
quently to prevent infection and maintain lubri- causing underestimation of the actual extent
cation of the wound. Management of an eyelid of the laceration.
laceration is undertaken after the management • Inspect for tissue loss, although this is an
of any globe injury.2 If the globe is ruptured or unusual circumstance. Most of the time soft
lacerated, repair of the eyelid laceration is typi- tissue edema and retraction of the tissues
cally deferred to prevent undue pressure on the contribute to a false appearance of tissue loss.
wounded globe. If the eyelid laceration is not Once the edema subsides and the deeper
edematous and the wound can be reapproxi- tissues are reapproximated, superficial tissues
mated without tension, it can be repaired during tend to fall into place and the cut edges of the
the same visit to the operating room but after skin fit together like pieces of a puzzle.
globe repair. • Preserve and restore eyelid anatomy and
General anesthesia is recommended for most function.
children because they may not tolerate probing
of the injured tissue or local injection of NON-MARGINAL EYELID LACERATIONS
anesthetic. Older children and adult patients
with significant anxiety can benefit from local Inspection, as described above, is vital when
anesthetic with sedation (often an oral ben- approaching eyelid lacerations. Gently pulling
zodiazepine). However, most adult patients tissues apart and probing their extent is vital to
can tolerate local anesthesia without sedation. properly close all layers and prevent retention of
We routinely use lidocaine 2% with epinephrine foreign bodies. Depth of injury is particularly
to allow anesthesia with vasoconstriction. vital. If preaponeurotic fat is encountered, this
Epinephrine should be avoided in patients indicates that the orbital septum has been vio-
with uncontrolled hypertension or cardiac lated. If the upper lid is involved, the wound is
arrhythmias. inspected for a laceration of the levator aponeu-
When planning repair of eyelid lacerations, rosis. If the levator aponeurosis is injured and the
general principles to take into consideration patient has blepharoptosis, an oculoplastic spe-
include: cialist should be consulted for defi nitive repair.
• Assemble a surgical team that is familiar with Vertical aponeurotic tears usually heal without
ophthalmic instruments. treatment and do not require suture repair.
• Protect the globe. Plastic or metal protective
covers are commercially available and are Subcutaneous closure
placed on the eye before the eyelid repair to An absorbable suture such as 5-0 polyglactic acid
prevent inadvertent needle penetration. (Vicryl®, Ethicon, Somerville, NJ) on a spatu-
131
Ocular trauma
lated needle is our choice for deep tissue closure 5. Protect the eye. Sutures through the tarsal
in the periocular region. This suture can be used plate should be lamellar, especially overlying
for deep tissue closure above the brow. It can also the cornea, in order to prevent inadvertent
be used to anchor deep tissues to the periosteum abrasions or penetrations.
to take tension off the wound. There is no need to
place deep tissue sutures through the orbicularis Surgical repair
muscle beneath the brow unless required to • Clean, anesthetize, and inspect the eyelid
diminish tension on the skin sutures. It is also wound (Figure 9.5A).
unnecessary to suture the cut edges of the orbital • Freshen the lacerated edges and separate the
septum, as they will heal without treatment. anterior lamella from the posterior lamella
Most anterior lamellar defects can be closed using blunt dissection. Expose approximately
primarily. If there is tissue loss, an oculoplastic 3 mm of tarsal plate on both sides of the
specialist should be consulted since advanced wound.
techniques such as skin grafts or flaps may be • Approximate the tarsus by passing 5-0 poly-
necessary to appropriately close the defect. glactic acid sutures on a spatula needle through
partial thickness of the tarsal plate horizon-
Skin closure tally. Pass each suture approximately 2 mm
For most skin closures, the authors prefer 7-0 from the lacerated edge and exit mid-depth
nylon on a cutting needle below the brow and through the thickness of the tarsal plate. To
6-0 nylon above the brow. The nylon suture is prevent corneal or conjunctival abrasions,
preferred for skin closure because it creates the evert the eyelid after each pass to make certain
least amount of inflammation and scarring and sutures are not exposed on the posterior
it glides easily through the tissues. The suture is surface. Do not tie the knots until all sutures
typically removed in 1 week. Absorbable suture are in place, as this will make placement of
(e.g. 7-0 polyglactic acid) is advisable if follow- further sutures difficult. You may need as
up for suture removal cannot be assured or if many as two or three sutures passed in
suture removal might not be possible without similar fashion to properly realign the tarsus
anesthesia (e.g. in children). (Figure 9.5B). Leave the sutures untied and
direct attention to reapproximation of the
MARGINAL EYELID LACERATIONS eyelid.
• Pass a 5-0 silk suture at the level of the mei-
Primary closure, if possible, is the ideal proce- bomian glands in a vertical mattress fashion.
dure for repairing a marginal laceration. For This has been described as the ‘far-far-near-
eyelid defects under tension or in cases with near’ technique (Figure 9.5C). Take the fi rst
loss of tissue, oculoplastic consultation is typi- pass about 3–4 mm from the lacerated edge
cally necessary. When repairing marginal eyelid and exit in the same position on the other side
lacerations, similar goals are present for each of the wound. Begin the second pass on the
case: same side the fi rst pass exited, and pass the
1. Realign the eyelid margin. suture approximately 1 mm from the lacera-
2. Restore structural integrity of the tarsus. tion on both sides.
3. Avoid eyelid notching. • Tie the 5-0 polyglactic acid sutures to approx-
4. Minimize skin and deep tissue scarring. imate the tarsal plate (Figure 9.5D).
132
A B
C D
Figure 9.5 (A–E) Marginal lid laceration repair.
• Tie the silk mattress suture so the cut edges • Finally, close the overlying skin with inter-
slightly pucker. This will ensure good reap- rupted 7-0 nylon or vicryl sutures. Incorpo-
proximation and prevent lid notching. Leave rate the tag ends of the 5-0 silk to keep its
the tails of the silk suture long and incorpo- knot away from the cornea (Figure 9.5E).
rate them into the skin sutures to prevent the
knot from rubbing against the cornea.
133
Ocular trauma
CANALICULAR LACERATIONS 2. Inject dyed saline or viscoelastic through the

intact system and watch for passage of fluid
Any laceration in the region of the medial canthus through the lacerated end.
should be carefully inspected for the possibility 3. Inject air through the punctum and watch for
of a canalicular violation. If unsure whether the bubbles at the lacerated edge.
canaliculus is involved, the lacrimal punctum 4. If the proximal cut end of the canaliculus is
should be dilated and probed with a 0 or 00 still not apparent, insert a pigtail probe dipped
Bowman probe, taking care to avoid the creation in a steroid/antibiotic ointment through the
of a false passage. If the probe passes through the intact punctum and gently curve it around
system without any areas of exposure, the lacri- toward the injured canaliculus, following the
mal drainage system is most likely intact. normal anatomy. Look for the end of the
probe exiting the cut end of the canaliculus.
Surgical repair Care should be taken not to force the pigtail
Multiple options are available to repair canalicu- probe and create a false passage.
lar lacerations. These include the use of a mono- Once the cut ends are identified, repair pro-
canalicular stent, a bicanalicular donut stent, or ceeds. We will discuss each procedure
a bicanalicular Crawford stent. The stent allows individually.
proper realignment of the lacerated canalicular
edges and is usually left in place as long as 3–6 Monocanalicular stent
months. In the office setting, a Crawford stent is A monocanalicular stent (Mini Monoka; FCI
usually avoided as sedation is typically necessary. Ophthalmics Marshfield Hills, MA) can be used
A monocanalicular stent requires canulation of for lacerations involving the external 2/3 of one
only one canaliculus. This is particularly helpful canaliculus.
in the small percentage of people who do not • Identify the lacerated ends of the canaliculus
have a common canaliculus, a situation that as outlined above (Figure 9.6A).
renders placement of a donut stent difficult. • Trim the monocanalicular stent to the appro-
Bicanalicular stents such as the Crawford stent priate size so that the end of the stent rests in
and the donut stent are more stable and are less the lacrimal sac (approximately 12 mm).
likely to become dislodged prior to the intended • Dilate the punctum and advance the stent
removal and are the authors’ preferred method through both lacerated edges (Figure 9.6B).
of repair. • Approximate the deep soft tissues with inter-
For any method, the surgical site is cleaned, rupted 7-0 polyglactic acid sutures. Pass the
anesthetized, and draped. Attention is initially sutures adjacent to the cut ends of the cana-
directed at identifying the cut ends of the liculus for best approximation. If tension
canaliculus, fi rst inspecting the tissues with needs to be taken off of the wound, use 5-0
surgical loupes or an operating microscope. polyglactic acid.
The white sheen of the epithelial lined tube can • Close the overlying skin with interrupted 7-0
often be readily seen. If this is unsuccessful, polyglactic acid or nylon sutures.
several ‘tricks’ are available to identify the cut • Place two interrupted 8-0 vicryl sutures
ends: through both the medial and lateral ends of
1. Paint the area with a sterile fluorescein strip the stent footplate to fi xate the stent to the
to help visualize the cut ends. lid margin (Figure 9.6C).
134
A B
Figure 9.6 (A) A probe is used to identify the proximal

end of the lacerated canaliculus. (B) The monocanalicular
stent is inserted first through the proximal end of the
lacerated canaliculus before being trimmed and inserted
into the distal end of the lacerated canaliculus. (C) Final
appearance of the monocanalicular stent in place with
schematic drawing showing the final resting position of
the stent in relationship to the lacrimal drainage
anatomy.
Donut stent • Pass the opposite side of the pigtail probe

This method involves placing a silicone bicana- through the opposite punctum and exit
licular stent within the canalicular system utiliz- through the distal cut end. Thread the other
ing a pigtail probe. The use of the pigtail probe end of the 6-0 prolene into the islet and back
has been described previously not only for cana- the probe out, pulling the suture through the
licular lacerations but also for use in Moh’s punctum. The 6-0 prolene acts as a guide over
medial canthal reconstructions involving the which a silicone stent is placed.
lacrimal system. 3 • Using a piece of Crawford silicone stent
• Pass the pigtail probe through the intact cana- (remove the internal suture if present), thread
licular system and exit through the proximal the stent around the 6-0 prolene suture and
cut end. through the canalicular system. (Figure 9.7B)
• Thread a 6-0 prolene suture (needle removed) Coating the stent with an antibiotic ointment
through the islet of the probe (Figure 9.7A). may help slide the stent into position. Take
Back the probe out, pulling the suture through care not to bend the suture as kinks make the
the canaliculus. threading much more difficult. Advance the
135
Ocular trauma
A B
C D
Figure 9.7 (A) A pigtail probe has been placed through the upper punctum and exits the distal cut end of the
canaliculus. A prolene suture has been threaded through the tip of the probe. The schematic portion of the
figure details the path of the pigtail probe through the canalicular system. (B) Once the prolene thread has been
placed through both ends of the injured canaliculus, the suture is used as a guide for the silicone stent
placement. The schematic portion of the figure details the path of the stent through the canalicular system. (C) A
stripper is used to cut the silicone stent to the appropriate length without cutting the underlying prolene suture.
(D) Final appearance of the donut stent in place. The schematic portion of the figure details the final position of
the stent within the canalicular system.
stent into one punctum, through the lacerated step prior to tying the stent will prevent
edges and out of the opposite punctum. unnecessarily long stents that may rub against
• Grasp both ends of the silicone stent with a the cornea.
straight needle holder to prevent the suture or • After soft tissue closure, adjust the appropri-
stent from slipping out of the system. ate length of the stent by grasping the ends
• Once the canalicular system is fully cannu- with a straight needle holder. The silicone
lated with the stent and suture, direct your stent is trimmed to the appropriate length by
attention to reapproximation of the surround- removing the excess silicone tubing with a
ing soft tissues as described above. Taking this silicone stripper. The silicone stripper allows
136
the surgeon to score and separate the silicone canaliculus and down through the nasolacri-
tubing without cutting the underlying prolene mal duct in the same manner.
suture. Grasp the stripper with your index • Retrieve the stent underneath the inferior tur-
fi nger and thumb over the most inferior holes binate to complete the intubation of the cana-
of the instrument for better dexterity and licular system (Figure 9.8B).
control of the instrument. Pinch the instru- • Reapproximate the soft tissues surrounding
ment around the tubing and gently pull the canalicular laceration as described previ-
upwards (Figure 9.7C). ously. As stated previously, deep vicryl sutures
• Once the stent is trimmed to the appropriate should be placed as close to the cut ends of
length, tie the prolene suture within the stent the canalicular epithelium as possible for the
with three knots. best approximation of the tissues (Figure
• Rotate the knot into the lacrimal sac gently 9.8C).
using the forceps and needle holders (Figure • Grasp the stent with straight needle holders
9.7D). at the entrance of the nostril and strip away
the excess tubing with a stripper as described
Crawford stent above. This excess tubing can be sterilized
A Crawford stent is typically placed under local and saved for repair of canalicular lacerations
sedation. using donut stents as previously described.
• Identify lacerated ends of the injured canalic- • Tie the suture within the lumen of the Craw-
ulus as outlined above. ford stents to itself.
• Dilate the punctum and advance the stent • Anchor the Crawford stent to the nasal vesti-
into the punctum vertically for approximately bule using a 6-0 nylon or prolene suture
2 mm and then horizontally through the passed through the loop of the stent and then
proximal end of the lacerated canaliculus. through the lateral tissues just inside the nares
• Carefully cannulate the distal end of the (Figure 9.8D). This suture will prevent the
lacerated canaliculus with the stent. stent from prolapsing through the puncta and
• Advance the stent until a hard stop is encoun- will make future removal of the stent easier
tered (Figure 9.8A). since the ends can not retract into the naso-
• Redirect the stent vertically and advance lacrimal duct.
through the nasolacrimal duct. Use a large
Bowman probe inserted underneath the infe- POSTOPERATIVE WOUND CARE
rior turbinate to ensure the placement of the
probe through the lacrimal drainage pathway The newly repaired eyelid should be kept clean
is correct. If the space underneath the inferior and dry. Postoperative edema is diminished by
turbinate is limited, the turbinate can be infra- elevating the patient’s head to 30 degrees and
ctured with a Freer periosteal elevator. applying ice packs for the fi rst 48 hours following
• Retrieve the stent underneath the inferior surgery.
turbinate with a groove director such as the Pressure patching for up to 1 week, especially
Tse-Anderson Groove director (IOWA) or a after full-thickness laceration repairs, may be
Crawford hook. necessary to immobilize the lid and prevent
• Place the other end of the Crawford stent undue tension on the newly approximated
through the uninjured punctum, through the wound. Pressure patches should be avoided in
137
Ocular trauma
A B
C D
Figure 9.8 (A–D) Crawford stent placement.
138
children of amblyogenic age, following open 5. Proper antibiotic coverage and immunizations
globe repair, or in monocular patients dependent should be given preoperatively if necessary.
on the eye for activities of daily living. 6. If orbital fat is apparent in an eyelid wound,
Antibiotic ointment such as ophthalmic baci- the orbital septum may be violated, and sus-
tracin or erythromycin should be applied three picion for a laceration of the levator aponeu-
times daily for 1 week. A combination antibi- rosis is heightened.
otic–steroid ointment is typically used with 7. If there is any question regarding the struc-
canalicular lacerations to lessen scarring. The tural integrity of the canalicular system,
patient should be instructed to return if any each canaliculus should be probed individu-
unexpected swelling, pain, or secretions develop. ally with a small caliber Bowman probe.
Follow-up is scheduled for 5–7 days, at which 8. Repair of eyelid lacerations can be delayed
time permanent skin sutures are removed. Eyelid for 24–48 hours if necessary because of the
margin sutures should be left in place for 2 extensive vascularity of the involved tissues.
weeks. Stents are left in place for 3–6 months. If delayed, have the patient apply ice packs
Early removal may be necessary if cheese-wiring, and an antibiotic ointment to the wound
infection, or granuloma develop. several times a day.
9. Multiple methods are available to repair
canalicular injuries, the choice of which
SUMMARY depends on both the type of injury and
surgeon experience and preference.
1. Familiarity of eyelid anatomy is essential 10. Proper alignment of tissues with minimal
prior to eyelid laceration repair. tension on the wounds is the key to a suc-
2. Thorough cleansing and inspection of an cessful eyelid laceration repair.
eyelid laceration often requires injection of
local anesthesia. REFERENCES
3. Lacerated tissues must be separated to deter-
mine the full extent of the injury, since 1. Centers for Disease Control. Diphtheria, tetanus, and
fibrin can sometimes hold tissues together pertussis: recommendations for vaccine use and other
preventive measures: recommendations of the Immunization
giving the false impression of a more super-
Practices Advisory Committee (ACIP). MMWR 1991;40
ficial injury.
(No. RR-10):1–28.
4. Thorough inspection for retained foreign 2. Mindlin AM. Prioritizing the repair of adnexal trauma.
bodies and copious irrigation with a sterile Adv Ophthalmic Plast Reconstr Surg 1987;6:91–101.
solution is utilized for all eyelid lacerations 3. Jordan DR, Nerad JA Tse DT. The pigtail probe revisited.
prior to repair. Ophthalmology 1990;97:512–519.
139
10
orbital trauma
Vivian Schiedler, Thomas E. Johnson, Kenneth B. Krantz
INTRODUCTION PATHOPHYSIOLOGY
The orbit is the protector of the eye. Its unique Orbital injury can be classified into contusive or
pyramidal shape and thick bony walls serve to penetrating injuries, although significant overlap
protect the orbital contents (Figure 10.1). Orbital exists between the two. Objects that transmit a
injuries can occur alone or in combination with force to the eye and orbit without entering the
ocular trauma. In most cases, the treatment of structures cause contusive injuries. These objects
ocular trauma takes precedence over orbital and are typically larger than the size of the orbit, for
periocular injuries. Except for a few visually- example fi sts, balls, baseball bats, bottles, and
threatening orbital emergencies which require flat surfaces such as dashboards or doors. Even
immediate intervention to prevent permanent without direct tissue penetration by the object,
visual loss, the treatment of most traumatic orbital walls can be fractured and the globe can
orbital injuries can be postponed until after the be ruptured. Objects that pass through the
eye has been stabilized. In cases involving serious orbital or ocular tissues cause penetrating inju-
neurologic injury or airway compromise, the ries. These objects often have sharp or pointed
ophthalmologist must take the patient’s global edges, but dull or rounded objects can cause
medical status into consideration when prioritiz- penetration if sufficient velocity is present.
ing examination and treatment. Penetrating objects are often, though not always,
In this chapter we will discuss the examination smaller than the orbit in at least one dimension
techniques, diagnosis, and treatment strategies and include knives, pencils, twigs, bullets,
of the most common orbital injuries. umbrella tips, and nails. Injury is determined by
the structures that lie in the path of the pene-
EPIDEMIOLOGY trating object.
When evaluating the extent of injury, it is
Orbital trauma is reported to occur in multiple important to note both the mass and velocity of
situations. Motor vehicle accidents, altercations the object responsible for orbital trauma. The
with punches to the eye, falls, and sport injuries velocity of the object is more important than
involving impact with a ball are some of the its size since the energy causing tissue disruption
most common causes of trauma to the orbit. is determined more by the velocity than by
Young males typically account for the majority the mass of a projectile (kinetic energy = 1/2
of patients presenting with orbital trauma. mass × velocity2).1 Therefore, assuming similar
When due to motor vehicle accidents, orbital mass, high velocity objects have more kinetic
trauma is typically more severe in unrestrained energy and subsequently cause more tissue
passengers. damage.
141
Ocular trauma
Sphenoid bone The importance of a careful history cannot be

(lesser wing)
overemphasized, as serious orbital injuries may
Frontal bone externally appear trivial. Symptoms such as
decreased vision and diplopia should be specifi-
cally elicited. The timing and mechanism of
Sphenoid bone
injury should be specified. A past medical and
(greater wing) Ethmoid bone surgical history should be taken. Possible surgi-
Zygomatic bone Lacrimal bone cal intervention should be anticipated, so it is
Maxillary bone helpful to know the timing of the injury and the
Palatine bone
patient’s last meal, especially if general anesthe-
sia is a possibility. History of tetanus prophylaxis
may be relevant depending on the mechanism of
injury. A list of medications should be obtained.
Figure 10.1 The orbital floor is composed of the
Use of anticoagulants is particularly important
maxillary, zygomatic, and palatine bones, and is 0.5–
1 mm thick. The infraorbital neurovascular bundle
as it may explain relatively minor injuries with
travels along the middle of the floor, and most an unexpected amount of associated hemorrhage
fractures occur in the thin bone medial to the nerve. and help prepare the surgeon for possible intra-
The medial wall is composed of the maxillary, lacrimal, operative complications.
ethmoid, and lesser wing of sphenoid bones. The If available, visual acuity should be checked
ethmoid bone is very thin (0.2–0.4 mm), and is known
with a standard Snellen chart. Spectacle or
as the lamina papyracea. Most medial wall fractures
occur within the ethmoid bone. The frontoethmoid
pinhole correction should be used to obtain an
suture delineates the location of the cribriform plate. accurate result. In the emergency setting, near
The maxillary sinus lies beneath the floor, and the visual acuity using a near card will suffice.
ethmoid sinus lies medial to the medial wall. If the patient is unconscious, visual acuity
should be documented as soon as the patient
recovers the ability to cooperate with visual
EVALUATION testing.
Many traumatized patients have neurologic
Very rarely do patients present to an ophthal- deficits that impair vision testing, making the
mologist with life-threatening injuries. Occa- pupillary examination paramount. A relative
sionally patients experiencing sudden visual loss afferent pupillary defect in the absence of
in association with head or neck trauma may explanatory eye fi ndings should alert the exam-
ignore their more serious injuries and seek oph- iner to the possibility of orbital injuries compro-
thalmic care fi rst. It may become the ophthal- mising optic nerve function.
mologist’s responsibility to do a general physical Intraocular pressure is a vital test after orbital
examination to exclude the possibility of life- trauma. When orbital trauma leads to changes
threatening, non-ocular conditions, such as in intraocular pressure, it is typically elevated.
subdural hemorrhage. If injuries are limited to Mild transient elevations in intraocular pressure
the eye and ocular adnexae, ocular emergencies are seen with many cases of mild orbital edema.
(ruptured globe, intraocular foreign body, central Significantly elevated intraocular pressure in the
retinal artery occlusion) should be addressed absence of intraocular fi ndings should raise sus-
fi rst. picion of orbital causes. Orbital hemorrhage or
142
Closed globe injuries: orbital trauma
emphysema can be severe enough to cause orbital A

compartment syndrome.2
External examination is critical in determining
the type and extent of orbital injury. Evaluation
should begin with careful inspection of the
eyelid and periorbital skin. Periorbital lacerations
should be carefully explored to determine the
extent of injury and the possibility of intraorbital
foreign bodies. Small puncture wounds can
harbor deep intraorbital foreign bodies that are
not visible on examination (Figure 10.2). Ptosis
may be transient due to edema or hemorrhage,
or it can be relatively permanent if due to neu- B
rogenic injury. The degree of ptosis should be
measured and documented. Palpation of the
orbit for crepitus or bony discontinuity helps to
determine the presence of orbital fractures. The
position of the globe within the orbit should
be noted. Enophthalmos in the acute setting
suggests a large orbital floor fracture and meets
criteria for surgical intervention. Exophthalmos
suggests the orbital volume is increased by
edema, hemorrhage, bony fragments, and/or air.
Sensation in the distribution of the infraorbital
nerve should be specifically tested. Hypesthesia
of the cheek or upper lip may indicate an orbital
floor fracture and local injury to the infraorbital
nerve, although significant soft tissue swelling
may occasionally create temporary sensory
disturbances.
Inspection of the nasal passageway aided with
a nasal speculum should be performed in appro-
priate circumstances. Epistaxis is commonly seen
with orbital fractures. A clear liquid discharge
from the nose may be indicative of cerebrospinal
fluid (CSF) rhinorrhea, a rare but important sign Figure 10.2 (A) A 2-year-old boy was noted to have
that should alert the examiner to the possibility sudden onset of ptosis of the right upper lid. Closer
of fracture of the anterior cranial fossa and need examination revealed a small eyelid laceration. (B)
Exploration revealed a large intraorbital foreign body
for immediate neurosurgical consultation.
(pencil) that was removed without complication. The
Extraocular motility should be checked and
eye was unaffected.
any apparent deficits should be documented.
Acute diplopia in the setting of orbital trauma is
143
Ocular trauma
usually the result of extraocular muscle restric- and lateral wall are the thickest and are less
tion. This can be mild and transient if due to prone to fracture. The thinnest orbital bones are
orbital edema, but can also be more significant the floor medial to the infraorbital groove, and
and require surgical intervention if due to muscle the ethmoidal bone of the medial wall, the
entrapment within an orbital fracture. lamina papyracea. These thin walls separate the
A complete eye examination should accom- orbital contents from the maxillary and ethmoid
pany all assessments of an injured orbit. Specifics sinuses respectively. Contusive orbital injuries
of the examination for an injured eye are covered can lead to a ‘blowout’ of these thin regions. The
thoroughly in Chapter 3. Particular attention infraorbital nerve, a branch of the trigeminal
should be paid to the retina and optic nerve nerve, travels within the infraorbital canal along
examination. Elevated intraorbital pressure from the orbital floor, and exits through the infraor-
edema, hemorrhage, bony fragments, foreign bital foramen beneath the inferior orbital rim
bodies, and air can impede retinal and optic (Figure 10.3). This nerve is often traumatized
nerve perfusion. Sclopetaria, or retinal and cho- with orbital fractures, resulting in hypesthesia of
roidal rupture caused by concussive shock waves the cheek, side of nose, and teeth. The inferior
from a high-velocity intraorbital foreign body rectus runs along the orbital floor and is particu-
passing near the globe, can accompany penetrat- larly prone to entrapment following orbital floor
ing orbital trauma and should prompt investiga- fractures.
tion of retained intraorbital foreign bodies. 3
Commotio retinae, macular hole formation, and
choroidal rupture can also be seen with orbital
trauma.
Radiologic imaging is a vital component of the
orbital workup following ocular trauma and is
necessary to fully evaluate the extent of orbital
injury and its possible visual implications.
Imaging also assists in the development of the
most appropriate treatment strategy, including
neurosurgical and/or otorhinolaryngological
consultation. Computed tomography (CT) of Infraorbital
the orbits and surrounding structures (paranasal foramen
sinuses and intracranial cavity) is the study of
choice for evaluating patients with orbital
trauma. CT allows superior visualization of bony
structures, particularly the orbital bones and
contiguous sinus cavities.
ORBITAL BLOWOUT FRACTURES Infraorbital

nerve
Introduction Area of anesthesia

The orbits are pyramidal structures with thick, Figure 10.3 Course and sensory distribution of
sturdy bony rims that protect the eyes. The roof infraorbital nerve.
144
Pathophysiology Subcutaneous emphysema is the accumulation

Contusive orbital trauma is usually caused by of air beneath the skin due to a trauma-induced
fi sts, motor vehicle accidents, and small sports communication between the paranasal sinuses
ball projectiles, including tennis balls, racquet- and the orbit. One can often feel and hear a
balls, and baseballs. The term ‘blowout fracture’ crackling sensation when palpating the perior-
refers to the expansion of orbital volume due to bital tissues in this situation. Subcutaneous
the fracture of the thin orbital walls into the emphysema is often accentuated after the patient
adjacent paranasal sinuses. The quality of these blows his or her nose, forcing air into the tissues
thin bones is actually a protective mechanism, (Figure 10.4). The inferior rectus muscle or its
fracturing to lessen pressure on the globe and surrounding fibrous tissues are often entrapped
potentially prevent rupture of the eyewall. within the fractured bones of the orbital floor
There are two main theories regarding the resulting in restriction of ocular motility on
mechanism of blowout fractures. The ‘hydraulic upgaze (Figure 10.5) and resultant diplopia. This
theory’ suggests that there is an increase in muscle can also be swollen and hemorrhagic,
orbital hydrostatic pressure transmitted from resulting in decreased infraduction. One should
direct pressure on the globe, allowing the thin test sensation in the infraorbital nerve distribu-
bony walls to fracture before globe rupture tion, testing sensitivity of the cheek, side of nose,
occurs.4 The ‘buckling theory’ suggests that and teeth on the affected side. Gentle palpation
pressure directed against the sturdy orbital rim
causes a transient deformation of the bones with
resultant fracture of the thin orbital walls.5,6 A
Most likely both theories play a role in explain-
ing the etiology of these fractures. A ‘pure’
blowout fracture is one in which the orbital rim
is not fractured.
Evaluation
The examination for a potential orbital fracture
includes:
B
1. extraocular motility examination to detect
the presence of restrictions
2. external inspection for ecchymoses and
swelling
3. palpation for subcutaneous emphysema and
an orbital step-off
4. brief neurologic examination to detect the
presence of infraorbital nerve hypesthesia
5. measurement of relative proptosis or Figure 10.4 A patient with an orbital blowout fracture
was evaluated initially (A) and given appropriate
enophthalmos
instructions and follow-up. Several days later, he
6. slit lamp examination for subconjunctival presented with massive subcutaneous emphysema (B)
hemorrhage, conjunctival chemosis and and palpable crepitus after forgetting his instructions
further ocular injury. and vigorously blowing his nose.
145
Ocular trauma
Treatment
Systemic oral antibiotic therapy (typically a fi rst-
generation cephalosporin), nasal decongestants,
and ice packs are prescribed for the initial post-
traumatic period. One usually prefers to wait
7–10 days before initiating surgical treatment of
blowout fractures, allowing time for edema and
hemorrhage to resolve. Consultation with an
oculoplastic surgeon is necessary for defi nitive
surgical intervention.
Figure 10.5 Obvious upgaze restriction of the right eye is Initial diplopia is often due to hemorrhage and
seen on attempted upgaze following a blowout fracture
edema within the inferior rectus, and often
causing entrapment of the inferior rectus muscle.
resolves spontaneously. The timing and indica-
of the inferior orbital rim can detect a ‘step-off’ tions for surgical intervention have been
when the orbital rim is involved. Most patients debated.7–12 Indications for surgery include:
exhibit ptosis and proptosis initially due to post- 1. evidence of entrapment of the inferior rectus
traumatic edema and hemorrhage. Periorbital or its perimuscular tissues with diplopia
examination can reveal periorbital lacerations or 2. significant enophthalmos 7–10 days after
foreign bodies. About 10–30% of blowout frac- trauma (Figure 10.7)
tures are accompanied by other ocular injuries,
including corneal abrasion, traumatic hyphema,
iritis, ruptured globe, commotio retinae, retinal
detachment or retinal hemorrhage.6
When an orbital fracture is suspected, imaging
is required to confi rm the diagnosis. CT scan is
the procedure of choice (Figure 10.6). Axial and
coronal cuts are necessary to fully evaluate all of
the orbital walls, and thin sections are prefera-
ble. The medial floor and wall are inspected for
fractures and herniation of orbital contents into
the adjacent sinuses. Inspection of the bony apex
reveals the presence or absence of a posterior
ledge of non-fractured bone, an important fi nding
in planning the operative approach to the frac-
ture. The physician inspects the scans for associ-
ated facial fractures, including zygomatic and
roof fractures, as well as intracranial traumatic
injuries. Large fractures, or combined floor and Figure 10.6 Coronal CT scan reveals a displaced
fracture of the left orbital floor. The inferior rectus is
medial wall fractures, can result in significant
not entrapped within the sizable fracture, but it is
expansion of the orbital volume, a fi nding displaced inferiorly. Note the air–fluid level within the
that may influence the need for surgical maxillary sinus, a finding typical of orbital blowout
intervention. fractures.
146
with general anesthesia. The orbital floor can be

approached through either a transconjunctival or
a subciliary incision. The periosteum at the infe-
rior orbital rim is opened, and the periorbita is
gently elevated from the floor and medial wall.
The entrapped tissues are gently teased out of
the fracture using blunt instruments such as
Freer elevators. The surgeon attempts to fi nd the
posterior ledge of the fractured floor to enable
placement of an orbital implant (Figure 10.8).
Many materials have been used, including nylon
Figure 10.7 Severe enophthalmos of the right eye
following a large blowout fracture. Note the
sheets (Supramid), porous polyethylene, Teflon,
subsequent change in the upper eyelid sulcus and the bone, and others. The goal is to reconstruct the
downward displacement of the eye. normal contour of the orbital walls and reposit
the orbital tissues back into the orbital space.
3. injuries that are high risk for future Care is taken to avoid injury to the infraorbital
enophthalmos nerve that is easily seen running along the orbital
a. large fractures of the floor and/or medial floor. The medial wall can be approached through
wall the floor incision or through a transcaruncular
b. combined medial wall and floor fractures. incision. A medial wall implant is often neces-
If diplopia is persistent after 7–10 days, forced sary if a large fracture is evident in this area.
ductions are performed to verify muscle entrap- Small medial wall fractures usually do not need
ment. Anesthesia is applied to the limbus repair and rarely cause extraocular muscle
inferiorly, using topical lidocaine or tetracaine. entrapment. The periosteum is closed, as well as
The conjunctiva is grasped with forceps, and the the conjunctiva or skin. A silk traction suture
globe is elevated. A positive test is one in which may be left in the lower lid margin and taped to
the eye is not able to be elevated, indicating the forehead during the fi rst postoperative week.
entrapment of the inferior rectus, inferior This helps prevent lower lid retraction and offers
oblique, or the fibrous tissue surrounding these corneal protection during the immediate postop-
muscles. A forced generation test can also be erative period. Again patients are instructed not
performed to determine if muscle dysfunction is to forcefully blow their nose, and not to engage
due to swelling or hematoma within the muscle. in strenuous exercise requiring straining.
Again, the limbus is grasped with a forceps, and Some orbital fractures require urgent surgical
the patient is asked to look in the direction of intervention, and cannot wait the usual 7–10
action of the muscle in question (typically down days for edema and hemorrhage to subside. These
when the inferior rectus is the involved muscle). are the ‘trapdoor fractures,’ also described as the
The examiner can then determine if any muscle ‘white-eyed’ blowout fractures.13 This subtype
action is initiated. usually occurs in children and young adults sus-
It is much easier to correct enophthalmos early, taining an inferior wall break. This clinical sce-
as late enophthalmos is often complicated by nario is important to remember since emergent
orbital fat atrophy and shortening of the extra- consultation with an oculoplastic specialist may
ocular muscles. Surgical repair is accomplished be required. A hinged, non-comminuted floor
147
Ocular trauma
A recommended to identify heart block if symp-

toms are evident.16 Coronal CT may show an
‘absent’ inferior rectus, as the floor appears
almost normal with the muscle located in the
superior maxillary sinus. Scans may be read by
the radiologist as normal, so the physician should
personally examine the scans, and not rely on the
radiology report. The inferior rectus can rapidly
become ischemic, and ischemic necrosis can
result in fibrosis and permanent dysfunction.
Therefore, surgery within 24–72 hours is recom-
mended to prevent permanent damage to the
B
inferior rectus, and to lessen the risk of severe
bradycardia from the oculocardiac reflex.
The medial orbital wall is composed mainly of
the thin ethmoid bone, the lamina papyracea,
and is also easily fractured, with most medial
wall fractures occurring in conjunction with
floor fractures. Isolated medial wall fractures are
much less common and may be overlooked as
they uncommonly cause motility disturbances.
They are, however, a common cause of late
Figure 10.8 (A) Surgeon’s view of orbital floor fracture
enophthalmos. Complications of medial frac-
repair. An orbital implant has been placed to bridge the tures include medial rectus entrapment, orbital
gap created by the floor defect. (B) Surgeon’s view at emphysema, a pseudo-Duane’s syndrome in
the end of the case showing the small subciliary which the globe retracts and the fi ssure narrows
incision utilized during orbital floor fracture repair. on attempted abduction, and late enophthal-
mos.17 If a medial wall fracture is large, or if
fracture causes a tight entrapment of the inferior medial rectus entrapment occurs, surgical inter-
rectus or its perimuscular connective tissue. This vention is needed.18
fracture is thought to be similar to a ‘greenstick Orbital roof fractures can occur with signifi-
fracture’ in which the bones do not break com- cant trauma, usually after motor vehicle acci-
pletely, but fracture, bend, and quickly spring dents or falls from heights (Figure 10.9). These
back into an almost normal configuration due to fractures can involve the frontal sinus and intra-
the increased elasticity of the bones in younger cranial structures. Complications include CSF
individuals.14,15 The temporary deformity of the leak due to dural tears, intracranial hemorrhage,
floor allows the orbital tissue to become tightly ocular muscle imbalance with painful limitation
incarcerated. These patients demonstrate marked of upgaze, ptosis, traumatic encephalocele,
restriction on upgaze. Additionally, they can meningitis and brain abscess.19 A superior sub-
present with an oculocardiac reflex with nausea, periosteal hematoma can result in downward
vomiting, bradycardia and heart block. This con- displacement of the eye. Simple fractures of the
dition can be life-threatening, and an ECG is roof without inner table skull fracture can be
148
Lateral wall fractures are also caused by signifi-

cant trauma, usually after motor vehicle acci-
dents, falls, or assault with a blunt object. These
fractures rarely result in motility disturbance,
but may require repair if there is significant cos-
metic deformity, or if bony fragments impinge
on the orbital contents.
Trimalar fractures, also known as tripod or
tripartite fractures, involve the zygomatic bone.
Typically, fractures occur in three places: the
bone around the frontozygomatic suture, the
zygomatic arch, and the inferior orbital rim near
the zygomaticomaxillary suture. There is dis-
placement of the zygoma, with flattening of the
malar eminence, rounding and depression of the
lateral canthal angle, enlargement of the orbit
with enophthalmos, and hypesthesia of the cheek
and upper teeth (Figure 10.10). Cheek flattening
may be initially masked by facial swelling. The
fracture can extend to the orbital floor, with
Figure 10.9 Large, displaced orbital roof fracture with
entrapment of orbital contents and diplopia.
traumatic encephalocele formation in the superior
orbit. Patients often complain of difficulty chewing
(trismus) due to disruption of the temporoman-
repaired through a brow incision. More compli- dibular joint. Most surgeons recommend early
cated fracture requires neurosurgical and/or intervention in tripod fractures, as late repair is
otorhinolaryngologic consultation.20 difficult due to fibrosis of the tissues, and may
Nasoethmoidal fractures result from contusive necessitate osteotomies.
trauma to the mid-section of the upper face. The Midfacial fractures are divided into the Le Fort
nasal bones as well as the thin ethmoidal bones fractures. Le Fort I fractures involve the lower
fracture, with resultant widening of the intercan-
thal distance (traumatic telecanthus) and flatten-
ing of the nasal bridge. Fracture through the
lacrimal drainage system results in nasolacrimal
duct obstruction and tearing. Medial orbital wall
fractures can extend into the anterior cranial fossa.
These fractures often involve the cribiform plate
with penetration of bony fragments into the ante-
rior cranial fossa, and cerebrospinal fluid rhinor-
rhea. Neurosurgical intervention is often needed
for persistent CSF rhinorrhea.21 Repair of trau- Figure 10.10 Flattening of the malar eminence and
matic telecanthus or nasolacrimal duct obstruction rounding of the lateral canthal angle associated with a
can be performed by an oculoplastic specialist. tripod fracture.
149
Ocular trauma
aspect of the maxilla, and do not involve the single binocular vision in primary position, and
orbit. Le Fort II fractures, also called pyramidal blepharoplasty of the opposite upper eyelid to
fractures, involve the maxilla, nasal bones, infe- mask the enophthalmos of the traumatized
rior orbital rims, medial orbital walls and floors, side.7,8
and lacrimal drainage systems. A Le Fort III
fracture, also known as craniofacial dysjunction,
involves the nasal bones, medial and lateral INTRAORBITAL FOREIGN BODIES
orbital walls, and zygomatic arches, with the
facial skeleton connected to the cranium only Introduction
with soft tissue. Orbital involvement in types II The majority of intraorbital foreign bodies are a
and III can result in extraocular muscle entrap- result of assault, industrial accidents, or freak
ment and diplopia. accidents at home, at work, or during recreational
Early postoperative complications of floor and activities (Figure 10.11).24 Both sharp and blunt
medial wall fracture repair include infection, instruments have been responsible for vision loss
bleeding, loss of vision, and diplopia. If the and even death from intracranial extension.
orbital implant is too large, optic nerve compres- Examples include knives, scissors, pencils,
sion at the orbital apex can occur. Patients with bullets, BB pellets, fi shhooks, umbrellas, and
an entrapped muscle often have transient post- twigs, to name but a few.
operative diplopia due to hemorrhage and edema An intraorbital foreign body should be sus-
within the muscle. Patients with older fractures pected in patients with a remote or recent history
can have scarring and fibrosis of the inferior of trauma, no matter how trivial. Patients may
rectus, and even with complete release may con- not recall a specific traumatic event. They may
tinue to be diplopic. Strabismus surgery may be not seek medical care for small lacerations or
needed to re-establish single vision in this group puncture wounds until acute inflammation from
of patients. Adequate time after surgery, usually a retained foreign body arises. A high index of
6 months, is needed to allow postoperative suspicion is especially important in evaluating
recovery of muscle function before strabismus children with periocular inflammation. Signs
surgery is contemplated. and symptoms of retained intraorbital foreign
Late complications are usually related to the bodies include:25–28
orbital implant. They include infection, migra- 1. orbital mass
tion, and extrusion.22 Additionally, intraorbital 2. proptosis
inclusion cyst can occur, especially if sinus 3. painful or restricted eye movements
mucosa remains in the orbit after wall repair. 4. gaze-evoked amaurosis
Rarely, a late bleed into the capsule surrounding 5. diplopia
the implant occurs, and patients report pain, 6. ptosis
a pressure sensation, inflammation, and 7. lagophthalmos
proptosis.23 8. draining sinus tract
Repair of old fractures is more difficult, as 9. orbital cellulitis.
they are usually complicated by fibrosis of the
entrapped tissues as well as fat atrophy. However, Pathophysiology
good results can often be obtained. Other surgi- The size, site, and mechanism of entry as well as
cal options include strabismus surgery to restore the velocity and composition of the foreign body
150
A bismus, while damage to the angular artery or

vein can result in profuse bleeding or hematoma.
Low-velocity objects such as BB pellets can
sometimes enter the orbit without significant
collateral damage to adjacent structures and
can remain indefi nitely within the orbit without
complication. However, high-velocity objects
such as rifle or gunshot bullets often cause severe
intraorbital tissue disruption. Gunshot injuries
through the retrobulbar space often damage the
B extraocular muscles, optic nerve, and surround-
ing blood vessels, resulting in extreme proptosis
due to massive edema, hemorrhage, and loss of
normal globe attachments.
Diagnostic and therapeutic decisions are guided
in part by the composition of the suspected
foreign body. Most metals (lead, steel, alumi-
num) are inert and cause relatively little orbital
damage in the absence of infection. Copper,
however, tends to cause chronic inflammation
and can incite purulence even after a period of
Figure 10.11 ‘Freak’ accidents account for a large quiescence. Glass and stone are inert materials
percentage of intraorbital foreign bodies. A 27-year-old and are usually well tolerated within the orbit.
male was at work when he was inadvertently injured On the other hand, organic matter is poorly toler-
with a nail gun (A). The nail is seen entering in the
ated as it often incites a marked inflammatory
brow line. A plain X-ray shows the depth of the nail into
the orbit (B). Unfortunately, the nail had entered the response, is more often associated with infection,
eye, creating a globe laceration and extensive retinal and can lead to persistent draining fistulous
detachment. Despite repair, vision remained hand tracts. Retained wooden foreign bodies can
motions. decompose, fragment into smaller pieces, create
chronic fi stulas, migrate deeper into the orbit or
self-extrude after migrating to the surface.28
often determine symptomatology. As would be
expected, large foreign bodies are more likely to Evaluation
cause more extensive tissue destruction than Metallic foreign bodies are generally well visual-
smaller ones. However, the location of injury also ized on CT whereas organic matter such as wood
matters. Objects penetrating the superior orbit can be mistaken for air or fat on CT. Magnetic
are more likely to extend into the intracranial resonance imaging (MRI) is the imaging modal-
cavity through the superior orbital fissure or the ity of choice for suspected intraorbital wooden
orbital roof.26 Children are at particular risk of foreign bodies, but they can still be missed, par-
extension into the anterior intracranial fossa ticularly if small. MRI is contraindicated when
due to lack of frontal sinus development. Medial metal is suspected due to possible mobilization
injuries can damage the trochlea, leading to stra- of the foreign body against critical structures.
151
Ocular trauma
Thin axial and coronal views should be obtained Indications for observation of intraorbital foreign
to determine the exact location of the foreign bodies include:
body and to assess the status of the cranial vault 1. small, smooth, inert, posteriorly-located intra-
and contiguous paranasal sinuses. To help guide orbital foreign bodies
surgical planning, special attention should be 2. absence of infection or inflammation
paid to affected structures, depth of the foreign 3. lack of current or potential visual
body, and extension into extraorbital spaces. compromise
Extension into contiguous sinus cavities may 4. high risk of iatrogenic injury during surgical
require a combined approach with ophthal- removal (hemorrhage or functional deficit)
mology and otorhinolaryngology. Intracranial that outweighs the benefit of removal.
involvement via the superior orbital fissure, the When observation is elected, patients should be
optic canal, or an orbital roof fracture can be monitored closely during the fi rst year for stabil-
life-threatening, requires a high index of suspi- ity. They should also be warned of the risk of
cion to diagnose, and demands neurosurgical dislodgement should they ever develop an impor-
intervention when discovered.26 tant indication for MRI (if the foreign body is
Because the orbit converges toward its apex, metallic).
long pointed objects can be directed toward the Intraorbital vegetable matter should be removed
apex by the confi nes of the bony walls. The expediently and thoroughly. Aggressive irriga-
deeper the foreign body penetrates, the more tion with antibiotics and debridement of sur-
likely a serious injury will result. Sometimes the rounding tissues is vital. Intraoperative cultures
patient will have removed a deeply penetrating should be obtained with dirty wounds and inju-
foreign body prior to examination. When the ries involving organic material. Wounds caused
history or clinical fi ndings suggest a deep orbital by wood (twigs, pencils, golf tees) often carry
injury, a minor-appearing external wound should and deposit multiple small organic particles
not fool the examiner into overlooking a more through the path of entry. Complete removal
serious underlying injury. Vital structures such can be difficult, especially since these particles
as the optic nerve, ophthalmic artery, and sensory can break into smaller pieces that are poorly
and oculomotor nerves can be injured when an imaged even with MRI and wood has a tendency
object penetrates deep into the orbital apex. to catch on orbital tissues. Retained wooden
Serious and permanent injury, such as meningitis foreign bodies have a high incidence of granu-
or brain abscess, can result from unrecognized loma, abscess, or fi stula formation and can be
intracranial extension.26 extremely challenging to manage. It is important
to avoid pushing the decomposing and disinte-
Treatment grating pieces deeper into the orbit as they may
Indications for removal of intraorbital foreign become more difficult to remove with subse-
bodies include: quent efforts and cause iatrogenic damage.27
1. easily accessible anterior location Prophylactic antibiotics are controversial for
2. organic matter or copper small, inert intraorbital foreign bodies that are
3. inflammatory reaction not causing functional deficits. However, antibi-
4. sharp edges that threaten critical structures otic prophylaxis is indicated in cases of eyewall
5. impingement on extraocular muscles or nerves violation, sinocranial involvement, or exposure
causing functional deficits. to organic material.
152
CASE EXAMPLES
Case report: intraorbital foreign body (Figure 10.12)

A 2-year-old boy was vacationing with his family laceration was repaired. Incredibly, the globe was
when he fell from a second floor balcony into a bush. found to be intact. Cultures taken at the time of
The patient was airlifted to the emergency room for surgery grew Bacillus cereus. The patient was admit-
evaluation (A). Initial examination revealed a large ted for intravenous antibiotics. He steadily improved
twig extending from the orbit just below the left and never developed a clinical infection. The upper
globe (B). A CT scan with contrast revealed the twig eyelid healed well and final visual acuity was 20/20.
indenting and displacing the left eye superiorly. The (With permission from Johnson TE. Intraorbital
patient was taken to surgery where the foreign body Branch. From Arch Ophthalmol 2000;118:590–591.
was carefully removed (C) and the area thoroughly Copyright © 2000, American Medical Association. All
irrigated and debrided (D). An upper eyelid marginal rights reserved.)
A B
C D
153
Ocular trauma
TRAUMATIC OPTIC NEUROPATHY
Introduction
Direct optic nerve injuries are caused by penetrat-
ing orbital trauma resulting in contusion or tran-
section of the optic nerve by a foreign body, such
as a bullet or stab wound. Indirect optic nerve Figure 10.13 The optic atrophy seen in traumatic optic
injuries are caused by contusive head trauma. neuropathy is delayed by several weeks. A middle-aged
The most common mechanisms are motor vehicle male patient with a severe closed head injury had
fundus photos 3 days (left) and 3 months (right) after
accidents, falls, bike accidents, and assault.29 The
the initial injury. Visual acuity was hand motions at
incidence of optic nerve trauma as a result of both visits.
midfacial fractures is approximately 3%. 30
Most patients presenting with optic nerve
trauma are young, with a mean age of 32–34, and robulbar anesthesia, orbital apex surgery, or
approximately 81–85% are male. 31,32 Immediate reduction of midfacial fractures.
loss of vision upon impact is most common, but
some cases of delayed visual loss have been Evaluation
reported. No light perception vision upon initial By defi nition, indirect optic nerve trauma occurs
examination occurs in approximately 40–48% of in the setting of head trauma. Therefore, patients
cases. 31–33 A considerable number of cases are often have serious neurologic injury and must
associated with loss of consciousness with esti- be evaluated in conjunction with trauma phy-
mates reported around 45%. 31 Visual loss can sicians, neurosurgeons, and head and neck sur-
include loss of central visual acuity, visual field geons. If the patient is obtunded, the only clinical
defects, afferent pupillary defects and color evidence of a traumatic optic nerve injury may
vision defects. Profound visual loss is more be a relative afferent pupillary defect in the
common than mild visual loss. absence of globe injury. Evidence of optic atrophy
is delayed ophthalmoscopically for weeks to
Pathophysiology months following injury (Figure 10.13). However,
Damage to the optic nerve occurs by any com- every attempt should be made to document
bination of the following: visual acuity as soon as is clinically possible
1. direct deformation of the skull and optic and to rule out pre-existing visual loss by history.
canal The diagnosis of traumatic optic neuropathy
2. shearing of the optic nerve microvasculature cannot be made in the setting of normal visual
3. tearing of the nerve axons acuity or in the absence of a relative afferent
4. contusion of the nerve against the optic pupillary defect. While older reports in the
canal. literature suggested that all patients with trau-
The intracanalicular portion of the optic nerve matic optic nerve injuries presented with no
is the most vulnerable, in part owing to tethering light perception vision, more recent reports
of the dura by the periosteum of the optic canal. indicate that while most patients have visual loss
Iatrogenic optic nerve injuries can also occur of 20/400 or worse, some will present with mild
after ethmoidal endoscopic sinus surgery, 34 ret- visual loss. Therefore, a high index of suspicion
154
should be maintained to identify more subtle Although older literature suggests a grave
cases.29 prognosis with traumatic optic neuropathy,
Intraocular pathology may occur with or with- more recent literature demonstrates a 20–35%
out optic nerve injury and it may be difficult to improvement rate with no treatment. 35,36
distinguish the etiology of visual loss in these Several cases of spontaneous improvement
cases. However, decreased vision and abnormal despite severe vision loss (no light perception)
pupillary function without ocular injury is strongly have been reported 37 and this suggests that
suggestive of traumatic optic neuropathy. severe optic nerve trauma is not always
The diagnosis of traumatic optic neuropathy is irreversible. Observation alone may be reason-
clinical. Radiologic examination is useful in able for some patients, particularly for those
localizing the precise site and mechanism of with gastritis, diabetes, or immunosuppres-
injury and in preoperative planning. Computed sion as steroids can exacerbate any underly-
tomography is superior to magnetic resonance ing conditions and potentially lead to serious
imaging in detailing optic canal fractures or complications (e.g. GI bleeding, diabetic
impingement of the optic nerve by bony frag- ketoacidosis).
ments. MRI is superior in delineating optic nerve The rationale for treatment with high-dose
sheath hemorrhage. High resolution paraconal steroids is based on results from the second
oblique views may be necessary to distinguish National Acute Spinal Cord Injury Study
intrasheath from extradural hemorrhage. (NASCIS II). NASCIS II was a multicenter,
randomized, double-blind, placebo-controlled
Treatment study. It demonstrated that patients who received
The optimal treatment of traumatic optic neu- methylprednisolone (30 mg/kg initial dose
ropathy is unknown. Unfortunately, no random- followed by 5.4 mg/kg/hr) within the fi rst 8
ized controlled prospective trials have been hours after spinal cord injury had improved
feasible to date because of the difficulty in enroll- motor and sensory function when compared
ing traumatized patients, relative rarity of the to patients who received placebo, naloxone, or
condition, and controversy over optimal treat- high-dose steroids after 8 hours. 38 Animal
ment strategies. The biochemical and patho- models of spinal cord injury show that pre-
physiological mechanisms of optic nerve injury treatment with high dose methylpredniso-
are poorly understood and our knowledge in this lone prevents free radical damage and improves
area lags far behind our knowledge of brain and spinal cord blood flow. One animal model of
spinal cord injury. It is unknown whether current crush injury to the optic nerve showed preserva-
medical or surgical interventions improve the tion of optic nerve head blood flow when pre-
outcome when compared to the natural history treated with dexamethasone. 39 No prospective
of traumatic optic neuropathy. There is currently clinical studies similar to NASCIS II have been
no standard of care with regard to treating trau- feasible on patients with acute optic nerve
matic optic nerve injuries. injuries.
Management strategies currently include: High-dose methylprednisolone therapy for
1. observation traumatic optic nerve injury has recently been
2. high-dose corticosteroids called into question. Since the spinal cord is a
3. optic canal decompression. mixed gray and white matter tract and the optic
155
Ocular trauma
nerve is a purely white matter tract, the clinical fractures with bony fragment impingement
benefits of high dose steroid therapy may not of the optic nerve and for intrasheath
translate to the optic nerve. In addition, one hemorrhages.
recent animal study of crush injury to the optic In the future, neuroprotective agents may rev-
nerve showed a dose-dependent decline in the olutionize the treatment of acute optic nerve
number of surviving axons that were treated injuries. This will require a more complete
with methylprednisolone,40 suggesting a poten- understanding of the pathophysiologic mecha-
tial harm of this treatment. A recent prospective nisms of primary optic nerve injury and second-
randomized controlled trial on early high-dose ary mechanisms that perpetuate the damage and
methylprednisolone treatment after acute head contribute to the death of surrounding yet unin-
injury was actually ended early because cortico- jured axons.
steroids were found to have an adverse effect on It is difficult to predict an individual patient’s
survival.41 However, the mechanism by which prognosis following a traumatic optic nerve
corticosteroids may increase mortality in the injury. Although not always readily available,
setting of acute head trauma is unknown. In flash visual evoked potentials have been shown
summary, it remains unknown to date whether to have prognostic value in obtunded patients
high-dose methylprednisolone provides any with unilateral traumatic optic neuropathy and
benefit to the acutely traumatized optic nerve. in some cases may help guide management.42 It
The authors advocate using the NASCIS II is clear now that traumatic optic neuropathy
regimen only for stable patients with severe encompasses a spectrum of clinical outcomes
vision loss and without systemic contraindica- and the possibility for partial recovery is present.
tions. If there is no visual improvement within A poor prognosis is associated with:
2–3 days, the corticosteroids should be 1. no light perception vision immediately after
discontinued. trauma
Optic canal decompression may be of benefit 2. advanced age
to certain patients with delayed visual loss 3. a large relative afferent pupillary defect42,43
presumably attributable to secondary mecha- 4. impingement of the optic nerve by bony
nisms of optic nerve damage. Primary damage fragments
to optic nerve axons at the moment of injury 5. intrasheath hemorrhage that is not promptly
may be irreversible, but the subsequent cascade evacuated.
of inflammation, edema, ischemia, and meta-
bolic dysregulation within the unyielding ORBITAL HEMORRHAGE AND
bony optic canal may in turn further damage COMPARTMENT SYNDROME
surrounding axons. While no prospective studies
have proven this therapy to be clearly beneficial, Introduction
it is an accepted management strategy for Orbital hemorrhage is an uncommon entity,
patients who have no response to high dose but it can cause severe vision loss if managed
methylprednisolone, cannot be tapered from inappropriately. Patients typically present fol-
high dose methylprednisolone without loss of lowing facial trauma with pain and decreased
vision, or have stable visual loss followed by vision.
subacute worsening. Optic canal decompres- Trauma is the most common cause of orbital
sion should also be considered for optic canal hemorrhage. Other etiologies include:
156
1. Iatrogenic causes: the mechanism of injury should be undertaken

a. hemorrhage due to peribulbar or retrobul- if possible. Ophthalmic examination may reveal
bar injection reduced visual acuity, increased intraocular pres-
b. post-surgical bleeding. sure, an afferent pupillary defect, periorbital
2. Spontaneous causes: ecchymoses, subconjunctival hemorrhage, and
a. hemorrhage due to tumors conjunctival chemosis. Proptosis and taut orbital
b. hemorrhage due to vascular lesions. contents are universally present in orbital com-
Traumatic orbital hemorrhages may occur by a partment syndrome. In severe cases, choroidal
variety of mechanisms.2,44–50 The trauma can folds or evidence of a central retinal artery occlu-
either be directly to the orbit or to other sion may be present.45 A complete eye examina-
regions of the face with resulting fractures tion is necessary to rule out concomitant ocular
or secondary injury to the orbit. Bleeding may injury. Imaging of the orbits with CT or MRI is
occur within several spaces contained within the typically necessary. However, decreased vision or
orbit including the subperiosteal, extraconal, an afferent pupillary defect in the presence of
intraconal, or sub-Tenon’s space.45,47–50 Bleeding apparent orbital hemorrhage implies an acute
can also occur within the sheath of the optic orbital compartment syndrome. As permanent
nerve. damage to the optic nerve may result, emergent
The orbit is susceptible to compartment syn- therapy is critical, oftentimes before imaging can
drome because of its anatomy and small size. It be performed.45
is essentially a closed space bound by four bony If evidence of an optic neuropathy is present
walls and the minimally distensible orbital without significant clinical evidence of a retro-
septum and globe.2,50 Rapid elevation in com- bulbar hemorrhage, a CT scan may reveal a local-
partmental pressure can be created by a rela- ized radiodensity surrounding portions of the
tively small volume of hemorrhage since normal optic nerve. This may be indicative of an intra-
orbital volume is approximately 30 cc.46 Isch- sheath hematoma directly compressing the optic
emia of orbital tissues and increased intraocular nerve. An MRI scan should then be performed
pressure then occur depending on the extent of to confi rm the diagnosis.50 If an intrasheath
orbital hemorrhage. Orbital compartment syn- hematoma is present, the patient should emer-
drome is less likely in patients with extensive gently be referred to an oculoplastic surgeon for
orbital fractures, particularly large floor frac- possible optic nerve sheath fenestration.
tures, as orbital contents are decompressed into
the contiguous sinuses.
Treatment
Evaluation The treatment of orbital hemorrhage depends on
Patients affected by orbital hemorrhage may the severity of the compartment syndrome. Mild
report a variety of symptoms including decreased to moderate elevations in intraocular pressure
vision, pain, and diplopia.2,45,49 A multidisci- without evidence of optic nerve compromise
plinary approach is often necessary when dealing (afferent pupillary defect) can be treated with
with head trauma patients. Life-threatening con- glaucoma medications and observation. However,
ditions need to be ruled out and appropriate if the optic nerve or retinal circulation is com-
monitoring should be in place before evaluation promised, immediate defi nitive therapy is
of the eye begins. A thorough history regarding necessary.2,45,47,50
157
Ocular trauma
Initial emergency therapy is canthotomy and percent lidocaine with epinephrine is infi ltrated
cantholysis of the lateral canthal tendon. A thor- into the lateral canthal region both subcutane-
ough description of this procedure is found ously and subconjunctivally. If possible, 15
below. Lateral canthotomy and cantholysis works minutes should be allowed for the epinephrine
by increasing orbital volume and allowing the to take effect. If cautery is available it should be
eye to move anteriorly. Success is judged by at hand. If cautery is not available, the procedure
decreased intraocular pressure, improved visual should be performed using simple pressure for
acuity, and reversal of an afferent pupillary hemostasis.
defect. An inferior cantholysis is initially per- Clamping of the lateral canthus with a hemo-
formed. If further decompression is necessary, a stat may be performed to reduce the likelihood
superior cantholysis can also be performed. If of bleeding but usually is not necessary. A Stevens
the compartment syndrome is not alleviated by scissors is placed with one blade on the conjunc-
these interventions, emergent consultation with tival side of the lateral canthus and one blade on
an oculoplastic surgeon is mandatory. An oculo- the skin side of the lateral canthus. Lateral pres-
plastic surgeon can further decompress the orbit sure is applied to the scissors as the canthotomy
by using the following methods: is performed.
1. create a lid crease incision and open the orbital At this point the broad lateral canthal tendon
septum has been cut in half horizontally. There is little
2. explore the inferotemporal orbit through an decompression of the orbit as it has not been
inferior subciliary incision separated from the lateral wall of the orbit. To
3. surgically decompress the bony orbit. perform a complete inferior cantholysis, the infe-
Successful orbital decompression should be fol- rior lateral canthal tendon is strummed with the
lowed by careful monitoring as patients may scissors within the canthotomy wound. A fi rm,
redevelop orbital compartment syndrome if tense, cord-like attachment will be felt. These
further bleeding occurs. Lateral canthotomy and fi rm attachments are cut with scissors until the
cantholysis procedures are easily reversed by an lower lid becomes completely free from its lateral
oculoplastic surgeon once the acute episode has attachments. This may take several snips as
resolved. the lateral canthal tendon is wide and spreads
as it approaches the lateral orbital tubercle
Lateral canthotomy and cantholysis posterior to the lateral orbital rim. Hemostasis
If possible, proper informed consent is obtained. is obtained. The patient is then re-examined for
The region of the lateral canthus should be improvement in signs of orbital compartment
prepped and draped in a sterile fashion. Two syndrome.
158
CASE EXAMPLES
Case report: orbital compartment syndrome (Figure 10.14)

A 27-year-old male with a longstanding history of a lateral canthotomy was fashioned (B). After strum-
mental illness presented with decreased vision and ming the inferior crus of the lateral canthus with the
pain after attempting to self-enucleate his right eye. scissors to correctly identify its location, an inferior
Initial visual acuity was light perception without pro- cantholysis was fashioned (C). The lateral attach-
jection. Intraocular pressure was 60. Ophthalmic ments of the lower lid were visibly released (D). Intra-
examination revealed a total hyphema. The orbital ocular pressure after the procedure fell to 30. Despite
contents were tense and swollen (A). The lateral the measures, the patient progressed to no light
canthus and surrounding areas were sterilely perception vision due to massive suprachoroidal
prepped and draped. 2% lidocaine with epinephrine hemorrhage.
was used for local anesthesia. Using Stevens scissors,
A B
C D
159
Ocular trauma
TRAUMATIC EXTRAOCULAR
MUSCLE INJURY
Introduction
Extraocular motility disturbances are common
following orbital injury. Most are transient in
nature due to orbital edema and congestion. The
primary symptom is diplopia. If diplopia is
present, the examiner should determine if a
motility disturbance exists and whether the dip-
lopia improves or declines in certain directions
of gaze. Common causes of motility disturbances
following orbital trauma include:
1. orbital inflammation, edema, and congestion
2. orbital floor fracture causing entrapment of
the inferior rectus muscle
3. extraocular muscle laceration or avulsion
4. neurogenic injury
5. extraocular muscle hemorrhage (Figure 10.15)
or inflammation.
Neurogenic motility disturbances and extraocu-
lar muscle avulsions are rare. Direct damage to
the orbital muscle cone can affect multiple extra- Figure 10.15 Hematoma of the inferior rectus and
ocular muscles, cause severe motility problems orbital floor fracture associated with contusive orbital
injury.
and can be very challenging to repair.
Evaluation fact motility restrictions are permanent or

A motility examination is an important compo- transient.
nent of the complete ophthalmic examination.
With orbital injuries, upgaze and downgaze Treatment
restrictions are most frequently encountered. If Treatment of extraocular muscle injury varies
the patient is alert and cooperative, motility depending on the mechanism of injury. Ice packs
examination is as simple as asking a patient to and time typically lead to resolution of orbital
follow a moving object in the various directions congestion. When the inferior rectus muscle is
of gaze. If the patient is unable to cooperate with entrapped within an orbital floor fracture, repair
the examination, forced ductions can be utilized of the fracture typically corrects the diplopia.
to determine if a restriction defect is present. Extraocular muscle avulsion or laceration is par-
Motility examinations often improve signifi- ticularly difficult to repair and often requires
cantly in the fi rst 7–10 days following injury, tedious dissection to recover lost muscles.
mainly due to decreasing orbital congestion. This Persistent diplopia following corrective mea-
is one reason defi nitive management of orbital sures should prompt consultation with a strabis-
fractures is often delayed to determine if in mus specialist for defi nitive management.
160
SUMMARY 4. Smith B, Regan WF. Blowout fracture of the orbit. Am J

Ophthalmol 1957;44:733.
5. Fujino T. Experimental ‘blowout’ fracture of the orbit. Plast
1. The thinnest bones of the orbit (lamina papy-
Reconstr Surg 1974;54:81–82.
racea and orbital floor) are the most prone to 6. Kersten RC: Blowout fracture of the orbital floor with
fracture following contusive orbital injury. entrapment caused by isolated trauma to the orbital rim.
2. Blowout fractures of the orbit are a protective Am J Ophthalmol 1987;103:215–220.
mechanism to prevent undue force trans- 7. Putterman AM, Stevens T, Urist MJ. Nonsurgical management
mitted to the globe and to decompress the of blow-out fractures of the orbital floor. Am J Ophthalmol
1974;77:232–239.
orbit.
8. Putterman AM. Management of blow-out fractures of the
3. Clinical examination can often diagnose orbital floor: a conservative approach. Surv Ophthalmol
orbital fractures, but a CT scan is needed to 1991;35:292–298.
confi rm the diagnosis and allow appropriate 9. Dulley B, Fells P. Orbital blow-out fractures: to operate or not
surgical planning. to operate, that is the question. Brit Orthopt J 1974;31:47–54.
4. Repair of orbital fractures is usually delayed 10. Wilkins RB, Havins WE. Current treatment of blow-out
fractures. Ophthalmology 1982;89:464–466.
7–14 days after the initial injury to allow hem-
11. Hawes MJ, Dortzbach RK. Surgery on orbital floor fractures:
orrhage and edema to subside. influence of time of repair and fracture size. Ophthalmology
5. Indications for orbital fracture repair include 1983;90:1066–1070.
persistent diplopia, enophthalmos, or large 12. Burnstine MA. Clinical recommendations for repair of isolated
fractures. orbital floor fractures: an evidence based analysis.
6. Seemingly minor soft tissue injury can harbor Ophthalmology 2002;109:1207–1210; discussion 1210–1211;
quiz 1212–1213.
deep orbital wounds and retained foreign
13. Jordan DR, Allen LH, White J, Harvey J, Pashby R, Esmaeli B.
bodies. Intervention within days for some orbital floor fractures:
7. Traumatic optic neuropathy is a clinical diag- the white-eyed blowout. Ophthal Plast Reconstr Surg
nosis (relative afferent pupillary defect and 1998;14:379–390.
decreased vision, often with an otherwise 14. Bansagi ZC, Meyer DR. Internal orbital fractures in the
normal eye examination following trauma). pediatric age group: characterization and management.
Ophthalmology 2000;107:829–836.
8. The orbit is particularly susceptible to com-
15. Egbert JE, May K, Kersten RC, Kulwin DR. Pediatric orbital
partment syndrome because of its small floor fracture: direct extraocular muscle involvement.
volume and bony/septal enclosure. Ophthalmology 2000;107:1875–1879.
9. Lateral canthotomy and inferior cantholysis is 16. Sires BS. Orbital trapdoor fracture and oculocardiac reflex.
the procedure of choice for vision-threatening Ophthalmic Plast Reconstr Surg 1999;15(4):301–302.
orbital compartment syndrome. 17. Segrest DR, Dortzbach RK. Medial orbital wall fractures:
complications and management. Ophthalmic Plast Reconstr
Surg 1989;5:75–80.
18. Leone CR, Lloyd WC, Rylander G. Surgical repair of medial
REFERENCES wall fractures. Am J Ophthalmol 1984;97:349–356.
19. McLachlan DL, Flanagan JC, Shannon GM. Complications of
1. Dunya IM, Rubin PA, Shore JW. Penetrating orbital trauma. orbital roof fractures. Ophthalmology 1982;89:1274–1278.
Int Ophthalmol Clin 1995;35(1):25–36. 20. Flanagan JC, McLachlan DL, Shannon GM. Orbital roof
2. Linberg JV. Orbital compartment syndromes following fractures: neurologic and neurosurgical considerations.
trauma. Adv Ophthalmic Plast Reconstr Surg 1987;6:51–62. Ophthalmology 1980;87:325–329.
3. Shakin JL, Yannuzzi LA. Posterior segment manifestations 21. Beyer CK, Fabian RL, Smith B. Naso-orbital fractures,
of orbital trauma. Adv Ophthalmic Plast Reconstr Surg complications, and treatment. Ophthalmology
1987;6:115–135. 1982;89:456–463.
161
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22. Mauriello JA Jr, Hargrave S, Yee S, Mostafavi R, Kapila R. 38. Bracken MB, Shepard MJ, Collins WF, et al. A randomized,
Infection after insertion of alloplastic orbital floor implants. controlled trial of methylprednisolone or naloxone in the
Am J Ophthalmol 1994;117:246–252. treatment of acute spinal-cord injury. Results of the Second
23. Rosen CE. Late migration of an orbital implant causing National Acute Spinal Cord Injury Study. N Engl J Med
hemorrhage with sudden proptosis and diplopia. Ophthal 1990;322(20):1405–1411.
Plast Reconstr Surg 1996;12: 260–262; discussion 263. 39. Lew H, Lee SY, Jang JW, et al. The effects of high-dose
24. Simonton JT, Arthurs BP. Penetrating injuries to the orbit. corticosteroid therapy on optic nerve head blood flow in
Adv Ophthalmic Plast Reconstr Surg 1987;7:217–227. experimental traumatic optic neuropathy. Ophthalmic Res
25. Fulcher TP, McNab AA, Sullivan TJ. Clinical features and 1999;31(6):463–470.
management of intraorbital foreign bodies. Ophthalmology 40. Steinsapir KD, Goldberg RA, Sinha S, Hovda DA.
2002;109(3):494–500. Methylprednisolone exacerbates axonal loss following
26. Bard LA, Jarrett WH. Intracranial complications of penetrating optic nerve trauma in rats. Restor Neurol Neurosci
orbital injuries. Arch Ophthalmol 1964;71:332–343. 2000;17(4):157–163.
27. Liu D, Al Shail E. Retained orbital wooden foreign body: 41. Roberts I, Yates D, Sandercock P, et al. Effect of intravenous
a surgical technique and rationale. Ophthalmology corticosteroids on death within 14 days in 10008 adults with
2002;109(2):393–399. clinically significant head injury (MRC CRASH trial):
28. Wesley RE, Wahl JW, Loden JP, Henderson RR. Management randomised placebo-controlled trial. Lancet
of wooden foreign bodies in the orbit. South Med J 2004;364(9442):1321–1328.
1982;75(8):924–926, 932. 42. Holmes MD, Sires BS. Flash visual evoked potentials predict
29. Steinsapir KD, Goldberg RA. Traumatic optic neuropathy. visual outcome in traumatic optic neuropathy. Ophthalmic
Surv Ophthalmol 1994;38(6):487–518. Plast Reconstr Surg 2004;20(5):342–346.
30. Ashar A, Kovacs A, Khan S, Hakim J. Blindness associated with 43. Alford MA, Nerad JA, Carter KD. Predictive value of the initial
midfacial fractures. J Oral Maxillofac Surg 1998;56(10):1146– quantified relative afferent pupillary defect in 19 consecutive
1150; discussion 1151. patients with traumatic optic neuropathy. Ophthal Plast
31. Levin LA, Beck RW, Joseph MP, et al. The treatment of Reconstr Surg 2001;17(5):323–327.
traumatic optic neuropathy: the International Optic Nerve 44. Stern JH, Meyer DR. Orbital barotrauma. Ophthal Plast
Trauma Study. Ophthalmology 1999;106(7):1268–1277. Reconstr Surg 1995;11(1):49–53.
32. Levin LA, Joseph MP, Rizzo JF, 3rd, Lessell S. Optic canal 45. Bains RA, Rubin PA. Blunt orbital trauma. Int Ophthalmol Clin
decompression in indirect optic nerve trauma. 1995;35(1):37–46.
Ophthalmology 1994;101(3):566–569. 46. Krohel GB, Wright JE. Orbital hemorrhage. Am J Ophthalmol
33. Mauriello JA, DeLuca J, Krieger A, Schulder M, Frohman L. 1979;88(2):254–258.
Management of traumatic optic neuropathy: a study of 23 47. Liu D. A simplified technique of orbital decompression for
patients. Br J Ophthalmol 1992;76(6):349–352. severe retrobulbar hemorrhage. Am J Ophthalmol
34. Neuhaus RW. Orbital complications secondary to endoscopic 1993;116(1):34–37.
sinus surgery. Ophthalmology 1990;97(11):1512–1518. 48. McIlwaine GG, Fielder AR, Brittain GP. Spontaneous recovery
35. Seiff SR. High dose corticosteroids for treatment of vision loss of vision following an orbital haemorrhage. Br J Ophthalmol
due to indirect injury to the optic nerve. Ophthalmic Surg 1989;73(11):926–927.
1990;21(6):389–395. 49. Petrelli RL, Petrelli EA, Allen WE, 3rd. Orbital hemorrhage with
36. Lessell S. Indirect optic nerve trauma. Arch Ophthalmol loss of vision. Am J Ophthalmol 1980;89(4):593–597.
1989;107(3):382–386. 50. Rubin PA, Bilyk JR, Shore JW. Management of orbital trauma:
37. Wolin MJ, Lavin PJ. Spontaneous visual recovery from fractures, hemorrhage, and traumatic optic neuropathy.
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Am J Ophthalmol 1990;109(4):430–435.
162
11
Open globe injuries:
ruptures and lacerations
Daniel M. Miller, Charles W.G. Eifrig, James T. Banta
INTRODUCTION 1980 and 1986. 3 The economic impact, particu-

larly when considering loss of work days due to
In this chapter we will review the classification, injury, is immense.
epidemiology, evaluation, and management of The age distribution of severe ocular injury is
globe ruptures and lacerations. Case examples bimodal. Young males comprise the majority of
will reinforce key evaluation and management open globe injuries with patients aged between
points. 15 and 34 years old representing nearly one half
Guidelines for classifying mechanical eye inju- of all open globe injuries.2,4,5 The second peak is
ries were fi rst made uniform in the mid-1990s.1 seen in those over the age of 75.2,3,6 Falls are
A globe rupture refers to a full-thickness eyewall more common in this age group. Prior ocular
wound caused by a blunt object, while a lacera- surgery is also more common in the older popu-
tion refers to a full-thickness eyewall wound lation and may lower the threshold of force
caused by a sharp object. Specifics on the needed for a globe rupture to occur. For example,
classification of ocular trauma can be found in a contusive injury to an eye that has previously
Chapter 4. In this chapter we will discuss only undergone extracapsular cataract extraction,
globe ruptures and lacerations. Intraocular trabeculectomy, or penetrating keratoplasty may
foreign bodies are covered in Chapter 12. be more likely to cause rupture (Figure 11.1).
EPIDEMIOLOGY PATHOPHYSIOLOGY
It is difficult to estimate the number of open Distinct mechanistic differences exist between
globe injuries in the United States because of ruptures and lacerations, and these differences
significant variability in case reporting. However, have significant bearing on evaluation, operative
the involvement of an increasing number of planning, and repair. Ruptures are normally
hospitals and physicians in the World Eye Injury caused by blunt objects, have stellate, ragged
Registry (WEIR) will continue to improve our edges and frequently create significant intrao-
understanding of the incidence and prevalence cular disruption. Conversely, lacerations are
of open globe injuries. caused by sharp objects, have cleaner edges, and
A review of the National Hospital Discharge cause less intraocular disruption than com-
Surveys (NHDS) from 1984 to 1987 revealed an parably sized ruptures. Rupture sites are usually
incidence of approximately 4.6/100 000/year for located at the weakest point of the sclera. Figure
open globe injuries.2 In a smaller series in Alle- 11.2 shows the most common sites of globe
gheny County, Pennsylvania, the incidence of rupture. Surgeries with long incisions (extra-
open globe injury was 3.5/100 000/year between capsular cataract and penetrating keratoplasty
163
Ocular trauma
Figure 11.1 Penetrating keratoplasty wounds are a

common source of ruptured globes in the elderly,
particularly in association with repeated falls.
Figure 11.3 Although uncommon, small incision
phacoemulsification wounds can rupture, particularly if
the injury occurs within the first few months after
surgery.
EVALUATION
Severe eye injury often occurs as an isolated

event, but the presence of a potentially life-
threatening injury must be adequately ruled out
before proceeding with ocular examination.
Typically, in the emergency setting, a general
inquiry about the patient’s well being is made,
vital signs are recorded and a brief check of
mental status is attained. Once these basic steps
are completed and the patient is deemed in no
acute medical danger, attention can be directed
Figure 11.2 Globe ruptures most commonly occur just to the ophthalmic injury.
posterior to the insertion of the rectus muscles (red).
The fi rst step in evaluating a patient with a
Other common sites include previous surgical sites,
particularly extracapsular cataract surgery (blue) or
presumed open globe injury is a thorough history.
penetrating keratoplasty (yellow). In particular, the exact time of the injury, nature
of the injury or inciting object, and place where
the injury occurred should be documented. In
addition, if a patient reports a history consistent
wounds in particular) are prone to rupture, with a lacerating injury, it is important to ascer-
but even small incision surgical sites can tain whether the inciting object was removed,
rupture depending on the mechanism of injury displaced, or is in multiple pieces (e.g. shattered
(Figure 11.3). glass). In particular, it is critical to determine if
164
Open globe injuries: ruptures and lacerations
the potential exists for an intraocular foreign

body.
A complete past medical and ocular history is
crucial to perioperative planning. It is important
to obtain a basic assessment of the patient’s
general health because of the possible need
for intravenous sedation or general anesthesia
during surgical repair. In particular, has a recent
comprehensive examination been performed
by a primary care physician? What medical ill-
nesses are currently under treatment and are
these conditions stable? What specific medica-
tions are being taken? All past medical and
Figure 11.4 Video capture of massive extrusion of
surgical history should be investigated and
uveal contents (primarily retina) through a large
documented. Pre-existing ophthalmic disease corneal laceration. In this instance, minimal
and prior ocular surgery may be relevant to examination was necessary preoperatively. The eye was
the current injury or affect the surgical plan. covered with a metal shield until the time of surgery.
Drug allergies should be documented carefully.
Finally, the time of the patient’s last oral intake
is relevant to the timing of any surgical Common sense must play a significant role
intervention. when examining a severely injured eye. In the
A complete evaluation of the injured eye should case of an extensive globe rupture or laceration
then be performed. Fear and caution typically with obvious and extensive extrusion of intra-
accompany an examination of a known open ocular contents (Figure 11.4), a visual acuity,
globe injury as well as the potentially open globe. pupillary examination, and slit lamp examina-
Early in an ophthalmic career, the concern tion can be performed on the injured eye. A
centers on possibly missing an open globe injury. metal shield is then placed over the eye until
Systematic and complete eye examinations will further imaging studies (if necessary) and surgi-
prevent this error. The second component of cal intervention are undertaken. Again, the
concern involves inadvertently expressing globe uninjured eye must always be thoroughly exam-
contents through a rupture or laceration site. ined for a possible unrecognized injury.
Although this is a valid concern and all precau- Depending on the mechanism of injury, signifi-
tions should be made to prevent excessive manip- cant periorbital swelling can make ocular exami-
ulation of the eye and orbit, it is truly rare that nation very difficult. The use of eyelid retractors
an eye will be ‘over-examined’ to the point (e.g. Desmarres retractors) can allow safe visu-
where globe contents are put at risk. If anything, alization of the eye without causing unnecessary
passivity with a potentially open globe could pressure on the globe (see Chapter 3). Often, a
lead to a missed diagnosis. It is equally important trained staff member will hold the retractors
to remember that a comprehensive examination of while the examination is being performed by the
the uninjured eye is critical and must never be rel- ophthalmologist.
egated to another time. Unrecognized injuries can Visual acuity and pupillary examinations
and do occur in a seemingly ‘uninvolved’ eye. are vital and should be assessed at initial
165
Ocular trauma
presentation. Vision less than 20/400 and/or the When there is no obvious laceration or rupture
presence of a relative afferent pupillary defect after slit lamp examination, the IOP should be
(RAPD) often coexist with an occult globe measured, as relative hypotony is a key fi nding
rupture.7,8 A patient’s inability to provide an in the diagnosis of an occult open globe. We
accurate visual acuity due to I.V. sedation, intu- recommend that an ophthalmologist perform
bation, or intoxication should be documented in IOP measurement in the setting of a potential
the medical record. Visual acuity can be checked open globe. Anterior-to-posterior pressure on
with standard Snellen acuity in an eye examina- the globe or orbit should be minimized.
tion room, but a near acuity card may be used if A thorough slit lamp examination is then per-
the examination is in another setting. It is critical formed. The slit lamp exam is particularly helpful
to obtain the most accurate visual acuity possi- in diagnosing an open globe in the absence of an
ble, as initial visual acuity is an important prog- obvious rupture or laceration site. Several spe-
nostic indicator. Visual acuity should be measured cific examination fi ndings are often seen in this
with spectacles when possible. Pinhole acuity setting:
should be recorded if spectacles are unavailable. 1. 360 degrees of subconjunctival hemorrhage.
In eyes with severely limited visual acuity, the 2. 360 degrees of profound conjunctival chemo-
perception of hand motions should be tested in sis, also known as ‘jelly-roll’ chemosis (Figure
all four quadrants of peripheral vision. If hand 11.5).
motions vision is not found, perception of light 3. Relative asymmetry in anterior chamber (AC)
should be assessed with a bright light source (e.g. depth. If the globe violation is anterior to the
indirect ophthalmoscope). The differentiation ciliary body, the injured AC is frequently
between light perception and no light perception shallow, often with peaking of the iris towards
is very important, so the uninvolved eye should the wound (Figure 11.6). If the full-thickness
be completely occluded to prevent any test injury occurs in the posterior segment, the
errors. AC is frequently deeper than the fellow eye.
Assessment of pupillary function is critical
in the evaluation of the open globe patient and
may aid your assessment of the intubated or
sedated patient. The swinging flashlight test
with a bright light source such as the indirect
ophthalmoscope is used to detect an RAPD.7
In the setting of an irregular or fi xed pupil in
the injured eye (efferent pupillary defect), the
consensual response in the uninvolved eye can
be used to determine whether an afferent defect
is present (sometimes referred to as an ‘RAPD
by reverse’).
Intraocular pressure should always be recorded
in the uninvolved eye. Measuring intraocular
pressure in the injured eye may be deferred in Figure 11.5 ‘Jelly-roll’ chemosis is frequently associated
the case of obvious globe rupture or laceration. with open globe injuries.
166
or hyphema obscuring the pupil) or an extensive

anterior laceration with significant uveal pro-
lapse may sometimes preclude further examina-
tion. If the posterior segment cannot be visualized
or if the mechanism of injury (typically injury
with a blunt object or a fall) and examination
suggest a globe rupture but the rupture site
cannot be confi rmed, imaging studies can some-
Figure 11.6 A 23-month-old girl was accidentally
poked in the eye by her sister while on an airplane.
times aid in the diagnosis. Ocular ultrasound can
Examination revealed a peaked iris with iris be utilized in carefully selected cases provided
incarceration through a corneal laceration. A small the manipulation of the globe is minimal and the
hyphema was also noted. facilities and trained technicians are available.
Ultrasound has the advantage of providing spe-
cific anatomic information about the posterior
4. Transillumination defects of the iris can reveal segment including the presence or absence of
the path of small projectile injuries, often retinal detachment, choroidal hemorrhage, and
associated with perforations or intraocular intraocular foreign bodies. Computed tomogra-
foreign bodies. phy (CT) is better for ruling out metallic intra-
5. Violation of the lens capsule or focal cataract ocular foreign bodies, but offers less specific
formation can herald an open globe injury. anatomic information. Perforating injuries are
It is sometimes difficult to determine if an unique in that the fi nal resting place of the
anterior laceration of the cornea or sclera is full injuring object must be localized. Most objects
or partial thickness. In this case a Seidel test is remain within the orbital confi nes, but exten-
performed. The eye is anesthetized. A fluores- sion into the sinuses or even into the brain is
cein strip is dampened with sterile saline or possible.
topical anesthetic. At the slit lamp under cobalt Neither ultrasound nor CT is adequate to
blue light, the fluorescein strip is used to paint a completely rule out an occult eyewall violation.
dense coating of fluorescein over the wound. If If suspicion is high, surgical exploration is neces-
the wound is full thickness, a rivulet of aqueous sary. Our experience suggests that when explor-
will break through the fluorescein and cascade atory surgery is undertaken in questionable cases,
down the surface of the eye with a very charac- an eyewall violation is found in the vast majority
teristic appearance (Figure 11.7). of cases.
A dilated examination of the injured eye is Finally, it is crucial to exclude any concomitant
critical to rule out vitreous hemorrhage, intra- injuries to the lids, periorbital area, face, or head.
ocular foreign body, retinal detachment, and Concurrent orbital and adnexal injuries have
other concomitant posterior segment injuries. If been reported to occur in 25.7% of patients with
the possibility of a retained intraocular foreign open globe injuries. 9
body exists, further imaging tests are manda- Pediatric evaluation deserves a special mention.
tory. The following chapter discusses the diag- The normal difficulties encountered when exam-
nostic workup of a potential intraocular foreign ining young patients are often magnified in the
body in detail. Opaque media (e.g. total cataract face of severe ocular injury. All efforts are made
167
Ocular trauma
A B
Included
on DVD
Figure 11.7 A patient with a previous history of radial

keratotomy (RK) recently underwent cataract surgery.
Postoperatively, despite a formed anterior chamber, the
pressure was asymmetrically low in the operated eye. A
dense layer of fluorescein was painted over the area in
question using a moistened fluorescein strip (A). A
rivulet of aqueous was seen breaking through a violated
RK incision (B) and cascading down the surface of the
cornea (C), leading to this characteristic appearance of a
positive Seidel test.
to perform a safe, controlled examination of a for surgical exploration and/or repair are being
child with a potentially open globe. In the made.
authors’ experience, children often ‘grasp’ the
gravity of the situation and with the supportive PREOPERATIVE MANAGEMENT
encouragement and participation of family AND COUNSELING
members, a brief yet adequate examination can
often be performed at the slit lamp. However, After the examination is complete and the
maneuvers normally employed to examine an surgical plan is being formulated, avoid further
uncooperative child must be avoided in case an manipulation of the eye.10 A protective shield
open globe is present. In this situation, an exam- (e.g. Fox shield) is placed over the injured eye
ination under anesthesia (EUA) is often required (Figure 11.8) and the patient is instructed not to
to diagnose and potentially repair a full- eat or drink. Most anesthesia fasting guidelines
thickness eyewall injury. The potentially injured require no food or drink for a minimum of 6
eye should always be shielded while preparations hours before general anesthesia. According to
168
visual outcome in patients undergoing corneal or

corneal–scleral laceration repair emergently
versus postponing for a reasonable amount of
time so that appropriate operating room person-
nel or medical clearance can be obtained.16 One
study showed that a delay in repair of up to 36
hours does not impact postoperative visual
acuity.16 However, a recent study suggests that
for each day of delay in surgical repair there may
Figure 11.8 After confirmation of an open globe injury be a reduced visual prognosis.5 Intraocular
(pictured in Figure 11.6), a metal eye shield is taped foreign bodies should be removed promptly
into position to prevent further manipulation.
because of the increased risk of endophthalmitis
(see Chapter 12).
Local or general anesthesia may be utilized
the American Academy of Anesthesiologists’ depending on the mechanism of injury, the
practice guidelines, a 6-hour fasting period for extent of ocular injury, and the presence of coex-
a light meal and an 8-hour fasting period for a isting medical injuries. The use of periocular
meal consisting of meat, milk or fried foods anesthesia in ocular trauma is safe if performed
is recommended.11–14 However, many reports with careful case selection.17,18 Generally, the
support more liberal fasting guidelines in both authors prefer peribulbar anesthesia for adult
the adult and pediatric populations.11–14 patients with smaller anterior wounds without
Tetanus prophylaxis is generally recommended extensive uveal incarceration. All pediatric
if not current.15 If the globe is severely ruptured patients and more extensive open globe injuries
and disorganized with extensive loss of tissue require general anesthesia.
and the vision is no light perception, a primary Systemic antibiotics are recommended for
enucleation can be considered. Not uncommonly, open globe injuries unless the wound is small,
the patient may be in a poor psychological and/ well approximated, clean, and negative by Seidel
or physical state or even mentally impaired from testing. Typically, prophylactic intravenous anti-
illicit drugs or alcohol. The authors rarely recom- biotics consisting of vancomycin and a third
mend primary enucleation except in extreme generation cephalosporin are used to cover
cases with severe loss of tissue that cannot be the most common gram positive and negative
closed primarily (e.g. gunshot wounds). At a bacteria associated with post-traumatic endo-
minimum, attempted repair will allow the phthalmitis.19 Vitreous penetration of these anti-
patient time to understand the extent of injury biotics following trauma is adequate for most
and be better prepared for the psychosocial gram positive organisms.20,21 Oral antibiotics
aspects of enucleation. that have good vitreous and intraocular penetra-
Primary repair of open globe injuries should be tion may be considered in outpatient settings,
performed urgently, but timing may be deter- particularly fluoroquinolones.22,23 Generally, our
mined by the extent of ocular involvement, con- patients receive intravenous vancomycin and cef-
comitant bodily injuries, general health status, tazidime preoperatively followed by an oral
and operating room availability. Most studies fluoroquinolone and fortified topical antibiotics
have shown no significant difference in fi nal postoperatively.
169
Ocular trauma
The patient presenting with a severe ocular and surgical repair are described below within
injury has just incurred a potentially life-chang- each category of laceration or rupture.
ing event. The potential for a permanent loss of
vision and its attendant psychosocial issues must Corneal lacerations
be fully grasped by the surgeon and an appropri- Small, self-sealing, clean corneal lacerations
ately frank discussion with the patient and family without iris incarceration or other ocular injuries
must be undertaken.24 Realistic goals and a may be closed with cyanoacrylate glue.25 In our
guarded prognosis are topics to be broached experience, this represents a small subset of
before surgery. corneal lacerations. However, it may be an effec-
The Ocular Trauma Score was developed to tive way to stabilize a wound without a trip to
provide an objective guideline that predicts the the operating room. The key to this technique is
likelihood of visual recovery after severe eye to apply a uniform amount of glue to the wound.
injury.10 Ocular Trauma Score tables can be We utilize a combination of a cotton swab, baci-
posted in the examination rooms for easy refer- tracin ointment, and fi lter paper or plastic surgi-
ence and are helpful in providing patients and cal drape to serve as the glue applicator. By gently
families with concrete, objective data. The tables pressing on the cornea with this applicator the
can be seen in Chapter 4. glue is distributed evenly across the wound
(Figure 11.9). After removing the fi lter paper or
surgical drape, a bandage contact lens is placed
SURGICAL MANAGEMENT and topical antibiotics are prescribed. Close
observation is mandatory to make certain the
Repair of corneal lacerations, corneal–scleral glue stays in place and the eye remains formed
lacerations, scleral lacerations and globe ruptures and free of infection.
involves similar perioperative considerations. For larger or more complicated corneal lacera-
After sterile preparation of the eye, carefully tions, surgical management is required. The fi rst
avoiding undue pressure to the globe, the step involves creating a limbal paracentesis site
authors examine the eye under the operating with a paracentesis blade. A cohesive viscoelastic
room microscope and devise a surgical strategy. (preferred because of its easy removal without Included
on DVD
The goal of primary repair for an open globe extensive turbulence or vacuum) is injected
injury, whether rupture, penetration or perfora- through the paracentesis to stabilize the anterior
tion, is to: chamber, viscodissect iris incarcerated from
1. close the globe with minimal manipulation the wound, and protect the corneal endothelium
2. reposit or excise exposed intraocular and crystalline lens. Hyperinflation should be
contents avoided, particularly if the possibility of a pos-
3. explore the globe for unrecognized injuries terior rupture exists. A cyclodialysis spatula or
4. decrease the risk of endophthalmitis and the viscoelastic cannula is then inserted through
maximize the chance of functional recovery the paracentesis to free incarcerated iris or break
by restoring ocular integrity. adhesions. Balanced salt solution may also be
Obvious lacerations or rupture sites should be used to irrigate through the wound and free
repaired fi rst, usually proceeding from anterior incarcerated iris. If uvea appears necrotic or does
to posterior. The specifics of instrumentation not reposit easily, excision may be required.
170
A 10-0 Nylon suture

Cornea Corneal laceration
Figure 11.10 Appropriate architecture and depth of

corneal sutures during corneal laceration repair. Note
B the long pass and equal length on each side of the
corneal laceration, factors which minimize
postoperative astigmatism.
in halves at the pass of each subsequent suture.

Between 75% and 90% depth of suture pass is
optimal for healing and may lower infection risk
(Figure 11.10).26 Longer passes tend to induce
Figure 11.9 A small amount of bacitracin ophthalmic less postoperative astigmatism than short, tight
ointment placed on the end of a sterile cotton swab
sutures. The nylon sutures should be rotated and
acts as an adhesive to which a thin disk of surgical
drape, or, as in this case, pre-cut filter paper is attached. buried once the wound is stabilized and the eye
A thin, even layer of cyanoacrylate glue is then placed can maintain an adequate intraocular pressure.
on the surface of the filter paper. The glue is then Viscoelastic is gently irrigated out of the anterior
applied gently to the corneal wound (A). Once chamber at the completion of surgical repair.
removed, the thin, uniform layer of glue is seen closing Once the corneal laceration is repaired, proceed
the wound (B). A large scleral contact lens is then
to further globe exploration if warranted (see
placed to prevent inadvertent dislodging of the glue.
Ruptured globe repair, below). Subconjunctival
antibiotic and steroid is given upon completion
Once the wound is free of uvea, closure of the of the case. Topical antibiotic or combination
wound commences. 10-0 nylon suture is recom- antibiotic/steroid drops or ointment may be
mended for corneal lacerations and should begin applied before the eye patch and shield are
with a central suture. The wound is then divided placed.
171
Ocular trauma
CASE EXAMPLES
Case report: corneal laceration (Figure 11.11)

A 38-year-old Hispanic male was working on his car hemorrhage (A). No retinal tear or detachment was
when he felt something strike his left eye. He was not identified.
wearing protective eyewear. He reported immediate The patient was admitted to the hospital, intrave-
discomfort and decreased vision. Initially, he was nous antibiotics were initiated, tetanus immuniza-
evaluated at an outside emergency room. Informa- tion was given, and surgical consent was obtained.
tion obtained during this emergency room assess- The patient then underwent corneal laceration
ment included an orbital CT scan that did not repair and uveal repositioning. No intravitreal anti-
demonstrate an intraocular foreign body. He was biotics were administered. He was treated with
subsequently transferred for further evaluation and topical fortified vancomycin and tobramycin in the
treatment. first week postoperatively. He did not develop signs
On presentation, the patient’s visual acuity was or symptoms of endophthalmitis. The corneal lacera-
20/20 and hand motions in the right and left eye tion was well approximated following surgical repair
respectively. No relative afferent pupillary defect (B).
was detected. A complete examination of the right He had a diffuse vitreous hemorrhage after primary
eye including a dilated fundus examination was repair and a follow-up B-scan demonstrated a supe-
within normal limits. Slit lamp examination of the rior retinal detachment (C). A vitreoretinal surgeon
left eye revealed an extensive L-shaped corneal was consulted and the patient underwent a second-
laceration with uveal prolapse and 80% hyphema. ary procedure to remove the crystalline lens and
Intraocular pressure measurement was deferred. The repair the retinal detachment. A month later (just
iris, crystalline lens, and posterior segment were before suture removal), anterior segment examina-
poorly visualized through the hyphema and uveal tion revealed a well-healed corneal scar, extensive
prolapse. A B-scan ultrasound was obtained and loss of the temporal iris, and aphakia (D). However,
demonstrated diffuse fundus thickening with scleral his retina remained attached and final best-
folds, inferior vitreous opacities consistent with corrected visual acuity was 20/30 (with a rigid
posterior dislocation of the crystalline lens and gas-permeable contact lens).
A B
172
Case report: corneal laceration (cont’d)
C D
Corneal–scleral laceration the scleral wound is completely visualized.

Included
on DVD This is typically a larger wound with a higher Scleral wounds require a larger caliber suture,
incidence of uveal prolapse or incarceration. The typically 8-0 or 9-0 nylon. Large scleral lacera-
primary objective is to fi rst stabilize the limbus tions often have significant prolapsed uveal tissue
by placing a 9-0 nylon suture, thereby restoring that prohibits easy closure of the wound. Place-
the anatomy of the limbal ring. Once this is ment of one or two central sutures can stabilize
accomplished, repositing prolapsed uvea or the wound and allow more controlled reposition
relieving incarceration is possible utilizing the of prolapsed uveal contents. Toothed forceps
techniques described above. We generally repair (0.12) are used to grasp the edge of the wound
in an anterior to posterior direction after the while the suture is passed. Suture passes should
limbus is stabilized. Closing the scleral portion be at least 50% depth, and full-thickness passes
of the laceration will be discussed in the follow- should be avoided. Interrupted sutures are
ing paragraph. preferred, and the ends are cut and rotated if
possible.
Scleral laceration A scleral laceration may extend underneath or
Scleral wounds must be addressed with a high through a rectus muscle. In this case, the rectus
index of suspicion for a more extensive disrup- muscle may be secured with a double-armed 5-0
tion of ocular anatomy and prolapse of intraocu- Vicryl suture and disinserted from the globe (as
lar contents. The posterior extent of the laceration in standard strabismus surgery). The detached
must be identified. Overlying conjunctival and muscle is carefully secured away from the opera-
Tenon’s attachments are often edematous and tive field by marking the attached sutures with
adherent to the wound edges, obscuring the a bulldog-style clamp. Once the wound is closed,
extent of the laceration. It is critical to dissect a disinserted rectus muscle can be secured back
conjunctiva and Tenon’s with forceps and to its original insertion site with the pre-placed
blunt Westcott scissors so the posterior extent of double-armed suture.
173
Ocular trauma
Posterior scleral lacerations are technically Ruptured globe repair

more challenging. It may be necessary to perform The repair of a globe rupture is similar to what
a 360 degree conjunctival peritomy, isolate the has previously been described for lacerations of Included
on DVD
four rectus muscles on muscle hooks, and secure the cornea and sclera. Typically, ruptures are
each with a loop of 2-0 braided polyester suture. technically more challenging to repair since
This will permit maximal surgical exposure of stellate wounds, extensive loss of intraocular
the wound. To prevent further prolapse of uveal contents, and loss of tissue are much more
tissue, it is critical to limit torque or pressure on common. Oftentimes, exploratory surgery is
the globe while the laceration is open. If the necessary before the rupture site is located
wound continues posteriorly past the equator, since ruptures are often masked by extensive
complete closure of the wound may be difficult, hemorrhage and chemosis. A conjunctival perit-
especially since extensive manipulation may omy is performed in the area of suspicion using
lead to expulsion of ocular contents. In this forceps and blunt Wescott scissors, carefully
setting, the most posterior portion of the wound dissecting until reaching the rupture site. If the
may be left to heal by secondary intention. site of the wound is unknown, the peritomy is
If there is tissue loss, a scleral or corneal patch performed 360 degrees for maximum exposure.
graft is an option and should always be con- Bipolar cautery may be needed for hemostasis.
sidered in the preoperative assessment (so appro- It is critical to completely dissect away conjunc-
priate arrangements can be made with the eye tiva and Tenon’s attachments so that all aspects
bank). of the wound are visible. A muscle hook may be
If the mechanism of injury suggests a possible needed to help maneuver the eye for proper
perforating wound, exploration for both the exposure but extreme caution is warranted to
entry and exit wounds is mandatory. Frequently, prevent further extrusion of intraocular con-
the more anterior wound is discovered and closed tents. Suture selection can vary and depends on
fi rst. Exploration is then performed in the same the wound size, tissue loss, and location of
fashion as described above with isolation of each rupture. The authors prefer using 8-0 or 9-0
rectus muscle and gentle exploration of each interrupted nylon suture. Once the wound is
quadrant until the second wound (usually the found, it is closed in the same fashion as scleral
exit wound) is found and closed. lacerations described above.
The conjunctiva is closed with an absorbable Rarely, in cases of severe contusive trauma, a
suture. The authors prefer 6-0 plain gut or 7-0 circumferential rupture may exist that encircles
Vicryl. Subconjunctival antibiotics are given and a significant portion of the globe and passes
peribulbar anesthesia may be administered for beneath multiple rectus muscles. These injuries
postoperative pain control (particularly helpful require extensive dissection and disinsertion of
in children). multiple rectus muscles before the wound can be
adequately accessed and closed.
174
CASE EXAMPLES
Case report: globe rupture (Figure 11.12)

A 34-year-old white male was assaulted with a beer However, globe rupture was suspected because of
bottle 2 days prior to presentation. The patient the asymmetric intraocular pressure, 360 degrees of
reported immediate decreased vision and pain in subconjunctival hemorrhage (B), and an asymmetri-
the left eye. He was initially assessed at an outside cally deep anterior chamber (C) compared to the
emergency room where an orbital CT scan ruled out right eye. Examination of the posterior segment
an intraocular foreign body. He had no significant revealed only dense vitreous hemorrhage. The
medical or ophthalmic history. patient was consented for globe exploration and
On presentation his visual acuity was 20/20 OD and possible ruptured globe repair. At the time of surgery,
light perception OS. Thorough examination of the a 360 degree conjunctival peritomy was fashioned
right eye was normal. External examination revealed and muscle hooks were used to isolate the rectus
periorbital erythema, swelling, and multifocal skin muscles. A large rupture was identified starting
lacerations (A) around the left eye. Intraocular pres- beneath the insertion of the superior rectus and
sures were 18 and 5 in the right and left eyes respec- traveling circumferentially around the globe to
tively. Anterior segment examination of the left eye beneath the lateral rectus insertion. The total length
revealed no obvious corneal or scleral lacerations. of the wound was 17 mm. There was uvea,
A B
C D
175
Ocular trauma
Case report: globe rupture (cont’d)

vitreous, and retina prolapsed through the wound. total, complex retinal detachment (D). Vitreoretinal
Intraocular tissues were carefully reposited and the consultation was obtained and the patient subse-
wound was closed primarily with interrupted 8-0 quently underwent extensive posterior segment
nylon sutures. surgery to repair the retina and remove the cry-
His visual acuity remained light perception post- stalline lens. Postoperatively, the retina remained
operatively. Follow-up echography demonstrated a attached, but vision remained hand motions.
POSTOPERATIVE MANAGEMENT Corneal sutures are normally removed at the

slit lamp 1 month after primary repair. If second-
On the fi rst day after surgery, full clinical exami- ary procedures are necessary, suture removal can
nation is performed including intraocular pres- often be performed simultaneously.
sure check and dilated fundus examination. A Special consideration is necessary for the post-
Seidel test is performed on the wound if pos- operative care of pediatric patients. Depending
sible. Topical antibiotic, steroid and cycloplegic on the age of the patient, removal of sutures
drops are recommended. Aqueous suppressants often requires general anesthesia. Amblyopia is
are used if intraocular pressure is elevated. a feared outcome in children under the age of
The eye is shielded and recommendations to 10, even with an excellent anatomic result. Once
avoid strenuous activity are given. Oral antibiot- the acute phase following injury and repair has
ics, typically a fluoroquinolone, are continued. passed, consultation with a pediatric ophthal-
Follow-up is scheduled depending on the mecha- mologist is encouraged so that appropriate
nism, extent, and cleanliness of the inciting amblyopia management can be undertaken.
injury as well as the postoperative appearance
and intraocular pressure. Frequent follow-up is COMPLICATIONS AND OUTCOMES
needed in the case of uncontrolled intraocular
pressure or a case deemed high risk for post- As discussed previously, the Ocular Trauma
traumatic endophthalmitis. Small clean wounds Score can be helpful in preoperative counseling
with a good postoperative appearance can be and prognostication. Multiple studies have
followed in a week. Vitreoretinal consultation defi ned variables related to visual outcomes fol-
after primary repair is recommended in cases lowing open globe injury. Initial visual acuity has
with an intraocular foreign body, endophthalmi- been shown to be a good predictor of visual
tis, retinal detachment, posterior scleral rupture outcome in open globe injuries.27 The length
or laceration, vitreous hemorrhage, hemorrhagic and/or width of the laceration or rupture has
choroidal detachments, or a dislocated lens. been shown to correlate with outcomes as
Further descriptions of secondary surgery and well.28–33 In addition, lacerations posterior to the
further restoration of normal anatomy is beyond rectus muscles, vitreous hemorrhage, involve-
the scope of this text. ment of the crystalline lens, and the develop-
176
Figure 11.13 Visual recovery after corneal laceration repair often centers on correction of induced astigmatism.
A 53-year-old male underwent uncomplicated repair of an inferotemporal corneal laceration (A). Corneal
topography before suture removal revealed nearly 8 diopters of induced irregular astigmatism (B). After suture
removal, rigid gas-permeable contact lens fitting was performed with excellent visual results.
ment of a retinal detachment are poor prognostic in the unaffected eye and can cause permanent
signs.28–33 loss of vision. In a severely injured eye with little
Endophthalmitis following open globe injury is or no visual potential, the risk of sympathetic
a feared complication. The incidence of trau- ophthalmia must be discussed with the patient
matic endophthalmitis after penetrating ocular and be part of the decision-making process. The
trauma is low, occurring in approximately 5–14% specifics of sympathetic ophthalmia are dis-
of eyes. 34–40 The risk factors portending a greater cussed in detail in Chapter 13.
risk of endophthalmitis include intraocular Isolated corneal lacerations often have a better
foreign bodies, delay in wound closure greater prognosis than more extensive corneoscleral lac-
than 24 hours, injury in a rural setting, and dis- erations and ruptures. However, corneal scars
ruption of the crystalline lens.34–40 The most following laceration repair often lead to irregular
common organisms causing post-traumatic endo- astigmatism and frequently involve the visual
phthalmitis are Bacillus species, Staphylococcus axis (Figure 11.13). Rigid gas-permeable (RGP)
species, and other gram positive cocci. 34–40 Pro- contact lenses can often dramatically improve
phylactic intravitreal or intracameral injection of vision, even when the visual axis is involved. If
antibiotics (ceftazidime and vancomycin) is con- an RGP contact lens is unsuccessful, penetrating
sidered in patients with an intraocular foreign keratoplasty is often required for visual
body or a potentially contaminated wound. rehabilitation.
Traumatic endophthalmitis is discussed in detail
in Chapter 13. CONCLUSIONS
Sympathetic ophthalmia is a rare granuloma-
tous inflammatory disorder that usually occurs Open globe injury is one of the more harrowing
following ocular trauma. In these rare instances, diagnoses an ophthalmologist will face. A sys-
the injured eye incites an inflammatory response tematic approach to an injured eye is mandatory.
177
Ocular trauma
Proper classification, examination, counseling, 3. Landen D, Baker D, LaPorte R, Thoft RA. Perforating eye injury
repair, and postoperative management are im- in Allegheny County, Pennsylvania. Am J Public Health
1990;80:1120–1122.
portant to restore the eye’s anatomic integrity
4. Pieramici DJ, Macumber MW, Humayan MU, Marsh MJ,
and potential function. Despite appropriate de Juan E. Open-globe injury: update on types of injuries
intervention, the overall visual prognosis for and visual results. Ophthalmology 1996;103:1798–1803.
open globe injuries is very guarded. Prevention 5. Isaac DLC, Ghanem VC, Nascimento MA, Torigoe M,
remains the best treatment for all severe ocular Kara-Jose N. Prognostic factors in open globe injuries.
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6. Tielsch JM, Parver L, Shankar B. Time trends in the incidence
of hospitalized ocular trauma. Arch Ophthalmol 1989;107:
519–523.
SUMMARY 7. Levatin P, Prasloski PF, Collen MF. The swinging flashlight test
in multiphasic screening for eye disease. Can J Ophthalmol
1. Proper classification of open globe injuries has 1973;8:356–359.
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procedures.
1941–1944.
2. A complete and systematic examination of an 9. Hatton MP, Thakker MM, Ray S. Orbital and adnexal trauma
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of an open globe. Surg 2002;18:458–461.
3. Never ignore the fellow, seemingly uninjured 10. Kuhn F, Morris R, Witherspoon CD, Heimann K, Jeffers JB,
eye. Treister G. A standardized classification of ocular trauma.
Graefes Arch Clin Exp Ophthalmol 1996;234:399–403.
4. Specific examination fi ndings can aid in the
11. Warner MA, Caplan RA, Epstein BS, et al. Practice Guidelines
diagnosis of the open globe without a visible for Preoperative Fasting and the Use of Pharmacologic
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5. Perioperative planning (e.g. intravenous anti- Application to Healthy Patients Undergoing Elective
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www.asahq.org/publicationsAndServices/NPO.pdf
depending on the type and cleanliness of
12. Ljungqvist O, Soreide E. Preoperative fasting. Br J Surg
injury as well as the patient’s medical 2003;90:400–406.
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6. Surgical repair of the open globe strives to elective surgery? A national survey on current practice.
restore normal anatomy with minimal intra- Anesth Analg 2000;90:1348–1351.
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practices in pediatrics. Anesthesiology 1999;90:978–
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15. Benson WH, Snyder IS, Granus V, Odom JV, Macsai MS.
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21. Meredith TA, Aguilar HE, Shaarawy A, Kincaid M, Dick J, 32. Alfaro DV, Roth D, Liggett PE. Posttraumatic endophthalmitis.
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after intravenous administration. Am J Ophthalmol 33. Thompson WS, Rubsamen PE, Flynn HW, Schiffman J,
1995;119:774–778. Cousins SW. Endophthalmitis after penetrating trauma.
22. Hariprasad SM, Mieler WF, Holz ER. Vitreous and aqueous Ophthalmology 1995;102:1696–1701.
penetration of orally administered gatifloxacin in humans. 34. Alexander DA, Kemp RV, Klein S, Forrester JV. Psychiatric
Arch Ophthalmol 2003;121:345–350. sequelae and psychosocial adjustment following ocular
23. Hariprasad SM, Mieler WF, Holz ER. Vitreous penetration of trauma: a retrospective pilot study. Br J Ophthalmol
orally administered gatifloxacin in humans. Trans Am 2001;85:560–562.
Ophthalmol Soc 2002;100:153–159. 35. Vote BJ, Elder MJ. Cyanoacrylate glue for corneal perforations:
24. Gilbert CM, Soong HK, Hirst LW. A two-year prospective a description of a surgical technique and a review of the
study of penetrating ocular trauma at the Wilmer literature. Clin Exp Ophthalmol 2000;28:437–442.
Ophthalmological Institute. Ann Ophthalmol 1987;19:104–106. 36. Eisner G. Eye Surgery: An Introduction to Operative
25. Abu el-Asrar AM, al-Amro SA, al-Mosallam AA, al-Obeidan S. Techniques. New York: Springer-Verlag; 1990.
Post-traumatic endophthalmitis: causative organisms and 37. Sternberg P, de Juan E, Michels RG, Auer C. Multivariate
visual outcome. Eur J Ophthalmol 1999;9:21–31. analysis of prognostic factors in penetrating ocular injuries.
26. Olson JC, Flynn HW, Forster RK, Culbertson WW. Results Am J Ophthalmol 1984;98:467–472.
in the treatment of post-operative endophthalmitis. 38. De Juan E, Sternberg P, Michels R. Penetrating ocular injuries:
Ophthalmology 1983;90:692–699. types of injuries and visual results. Ophthalmology 1983;90:
27. Esmali B, Elner SG, Schork A, Elner VM. Visual outcome and 1318–1322.
ocular survival after penetrating trauma. Ophthalmology 39. Hutton WL, Fuller DG. Factors influencing final visual
1995;102:393–400. results in severely injured eyes. Am J Ophthalmol
28. Brinton GS, Aaberg TM, Reeser FH, Topping TM, Abrams GW. 1984;97:715–722.
Surgical results in ocular trauma involving the posterior 40. Groessl S, Nanda SK, Mieler WF. Assault-related penetrating
segment. Am J Ophthalmol 1982;93:271–278. ocular injury. Am J Ophthalmol 1993;116:26–33.
29. Reynolds DS, Flynn HW Jr. Endophthalmitis after penetrating
ocular trauma. Curr Opin Ophthalmol 1997;8:32–38.
179
12
Open globe injuries:
intraocular foreign body
James T. Banta, Jeffrey K. Moore
INTRODUCTION PATHOPHYSIOLOGY
Penetrating ocular trauma with retained intra- Entry into the eye by an IOFB usually occurs
ocular foreign body (IOFB) remains one of the because of small size, sharp edges, and rapid
most challenging and dramatic events encoun- velocity. This is particularly true in accidents
tered by ophthalmologists. The diagnosis requires involving hammering metal on metal, chiseling,
a detailed history and examination. Radiologic or operating a metal grinder. Small sharp objects
imaging is often necessary to confi rm the diag- with rapid velocity enter the eye with minimal
nosis. Once the diagnosis is confi rmed, appropri- disruption of surrounding tissues. Oftentimes,
ate management varies depending on the location small corneal or corneoscleral entry wounds will
of the IOFB and concomitant ocular injury. Con- be self-sealing.
sultation with a vitreoretinal specialist is recom- Conversely, large IOFB, particularly those
mended for management of posterior segment without sharp edges (e.g. BB), require a tremen-
foreign bodies. dous amount of force to enter the eye. The con-
cussive effect on the eye leads to tremendous
concomitant ocular disruption and poor visual
EPIDEMIOLOGY prognoses.
Nearly 2.5 million eye injuries occur annually in EVALUATION

the United States.1,2 Although IOFB injuries
make up only a small overall portion of these A high index of suspicion is vital when consider-
injuries, they contribute significantly to the cases ing an IOFB and history is a critical component
in which extensive surgical intervention is neces- of the ocular trauma workup. Several important
sary. An IOFB is present in 20–40% of penetrat- questions need to be posed:
ing ocular injuries. 3,4 The composition of the 1. When did the injury occur?
foreign body is most often metallic, ranging in 2. What was the mechanism of injury?
most reports from 86% to 96%.1,3,5–8 A multi- 3. Was eye protection in place at the time of the
tude of other substances have been reported accident?
including glass, plastic, and cilia. There is a 4. In an industrial accident, what type of mate-
strong predilection for these injuries to occur in rial was being worked with (e.g. iron, glass,
young, male workers, particularly those ham- wood, etc.)?
mering metal on metal.8–13 In a large case series The clinical history will raise or lower the sus-
of 297 patients with retained IOFB, 98% of picion of IOFB and will assist in guiding the
patients were male and 80% of accidents occurred subsequent examination and ancillary studies.
while hammering.11 The past medical history along with current
181
Ocular trauma
medication usage should be thoroughly reviewed. A

The time of last oral intake should be deter-
mined so that surgical intervention, if necessary,
can be timed appropriately. Tetanus prophylaxis
status should be determined.
Visual acuity should be documented and can
range from unaffected to no light perception.
While visual acuity has little usefulness in deter-
mining if an IOFB is present, it is an important
prognostic factor. Intraocular pressure is assessed
with care. A violated globe is often, but not
always, hypotonous relative to the fellow eye.
A host of related ocular fi ndings are often B
encountered concomitantly with an IOFB and
include:
1. subconjunctival hemorrhage
2. iris transillumination defect (Figure 12.1A)
3. hyphema
4. focal lens opacity (Figure 12.1B)
5. scleral laceration
6. corneal laceration
7. violation of the anterior and/or posterior
lens capsule
8. vitreous hemorrhage
C
9. intra- or subretinal hemorrhage
10. relative hypotony
11. deep anterior chamber compared to fellow
eye
12. visible foreign body (Figure 12.1C)
13. inferior focal corneal edema.
Slit lamp and dilated fundus examination are
crucial. A frank visible defect in the sclera,
cornea, iris, or lens capsule with direct visualiza-
tion of an IOFB secures the diagnosis. However,
scleral entry wounds are often obscured by Figure 12.1 Multiple examination findings assist in the
subconjunctival hemorrhage and the posterior diagnosis of intraocular foreign body including focal
segment is often obscured by anterior or poste- iris transillumination defects (A) and focal cataracts (B),
rior segment hemorrhage, making careful inspec- particularly when associated with a corneal or scleral
tion for an entry wound vital. Furthermore, the laceration (white arrow, B). Occasionally, a dramatic
presentation removes any diagnostic doubt (C).
possibility of multiple foreign bodies must always
be entertained. Seidel testing should be per-
formed on any suspicious wounds. Gonioscopy
182
Open globe injuries: intraocular foreign body
can sometimes reveal occult foreign bodies in the A

inferior angle (Figure 12.2) and is indicated when
a stable, full-thickness corneal wound without
violation of the anterior lens capsule or iris trans-
illumination defect is encountered. Transillumi-
nation is used to detect iris and lens capsule
defects and should be checked before (for iris
defects) and after (for lens capsule defects)
pupillary dilation if possible.
When examining an eye with a possible eyewall
violation, common sense must be used and
extensive manipulation avoided. Most contact B
examinations (applanation tonometry, gonios-
copy) can be performed with care if an entry
wound is very small and the eye is formed, as is
often the case with an IOFB. If a large eyewall
violation is present or the eye is clearly not
formed, manipulation of the eye is unwarranted
until the eye has been surgically stabilized. In
this situation, a limited examination is per-
formed, the eye is covered with a protective
shield, ancillary studies are performed to confi rm Figure 12.2 A young male construction worker
the diagnosis, and surgical intervention is complained of redness and pain several weeks
following a ‘minor’ accident at work. Initial anterior
undertaken.
examination showed only conjunctival injection and a
Ancillary testing is critical in the evaluation
few anterior chamber cells (A). Gonioscopy revealed a
and treatment of an IOFB. If the mechanism of metallic intraocular foreign body resting in the inferior
injury is suspicious and the examination incon- angle (B).
clusive, imaging should always be obtained in
order to rule out an IOFB. Plain radiography, the it has several shortcomings when compared
mainstay of diagnostic testing until the advent of to helical (spiral) CT scanning.16–18 Helical CT
computed tomography (CT), is no longer accept- scanning affords quicker scan times, less motion
able as a diagnostic procedure for suspected artifact, higher resolution, and less radiation
IOFB unless other modalities are unavailable. exposure. All CT scans ordered to locate an IOFB
Multiple studies have shown an unacceptably should be thin-cut sections, preferably 1 mm cuts
high false negative rate,14,15 particularly with if the suspected foreign body is small.
non-metallic foreign bodies. In the hands of an experienced ultrasonogra-
The current mainstays of IOFB localization are pher, ultrasound can be very useful in detecting
computed tomography and ultrasound. CT and locating an IOFB (Figure 12.4). Several pit-
remains the most commonly employed radiologic falls exist, however. Artifactual echoes can be
examination to determine if an IOFB is present misinterpreted as an IOFB (Figure 12.5).19
(Figure 12.3). Although conventional CT scan- Ultrasound overestimates the size of an IOFB
ning remains adequate for the detection an IOFB, and should not be used for this purpose. Ultra-
183
Ocular trauma
Figure 12.3 CT scan reveals a single posterior segment

foreign body. Thin axial and coronal cuts are necessary
to fully explore the globe for multiple foreign bodies.
sound is a technician-dependent technology and

should only be trusted if performed by a techni- Figure 12.4 B-scan ultrasound of two different patients
cian experienced in ocular ultrasonography. demonstrates an intraocular foreign body within the
Ultrasound biomicroscopy, although not always vitreous cavity (A) and within the substance of the
readily available, is a useful tool for detecting retina (B). Note the acoustic shadowing posterior to
both foreign bodies.
occult foreign bodies of the anterior segment.20
Magnetic resonance imaging (MRI) is not
appropriate for imaging and localizing IOFBs. shield (e.g. Fox shield) and encouraging the
The movement of ferromagnetic foreign bodies patient not to touch the eye are equally vital.
can induce significant migration21 and secondary Four primary goals are present when confront-
local ocular damage22 or even blindness.23 ing the IOFB patient:
All radiologic studies should be personally 1. preservation of vision
reviewed with a radiologist. 2. prevention of infection
3. restoration of normal eye architecture
TREATMENT 4. prevention of long-term sequelae.
Tetanus prophylaxis is given if not current. Most
The management of an IOFB begins even before surgeons prefer to begin prophylactic systemic
the diagnosis is confi rmed. Avoiding unnecessary antibiotics immediately. In the acute setting,
and extensive manipulation of an injured eye is they can be administered prior to and during
always important. Placement of a protective ancillary testing. Antibiotic selection should be
184
Figure 12.5 Intraocular air masquerading as IOFB. An Figure 12.6 Anterior chamber foreign bodies are
experienced ultrasound technician is vital in properly uncommon. Cilia as an anterior chamber foreign body
utilizing and interpreting ocular ultrasonography. is exquisitely rare.
directed towards the commonly encountered anterior lens capsule. Viscoelastic can also be
organisms found with open globes. Antibiotic used to manipulate and move small foreign
use is controversial and is covered later in this bodies, providing for safe and efficient removal.
chapter. If visualization is problematic, a surgical gonios-
The fi nal resting position of the IOFB and the copy lens (e.g. Koeppe lens) is utilized to directly
degree of concomitant injury determine the visualize the foreign body to lessen the risk of
approach and extent of surgical intervention. iris damage with blind attempts at grasping the
Anterior chamber, intralenticular, and posterior IOFB. Once the foreign body is localized, it is
chamber foreign bodies raise different surgical grasped under direct visualization with forceps
challenges and management considerations. and removed through the limbal incision, enlarg-
ing as necessary. Bimanual techniques are some-
Anterior chamber foreign bodies times needed to extract a foreign body imbedded
One-quarter to one-third of IOFBs will remain in the iris. A metallic foreign body can some-
anterior to the posterior lens capsule11 (Figure
Included
times be removed with an intraocular magnet. on DVD
12.6) and are technically less difficult to remove

than posteriorly situated foreign bodies. Entry Intralenticular foreign bodies
wounds through the cornea or limbus are cleared Intralenticular foreign bodies (ILFB) are not
of any prolapsed iris, always favoring reposition commonly encountered, accounting for only 7–
of viable uvea if feasible. Closure of the wound 10% of all intraocular foreign bodies. Most intra-
with 10-0 nylon sutures as described in the pre- lenticular foreign bodies are removed at the
vious chapter is then performed. Once the ante- time of injury in hopes of preventing infection,
rior chamber is closed, a limbal paracentesis or inflammation, secondary cataract, or siderosis
a beveled clear corneal incision is created several (Figure 12.7). Lens capsule breach significantly
clock hours away from the foreign body. Visco- increases the risk of post-traumatic endophthal-
elastic is used to maintain the anterior chamber mitis.24 Surgical removal of an intralenticular
depth and protect the corneal endothelium and foreign body has been well described. When
185
Ocular trauma
A B
Included
on DVD
Figure 12.7 A young male patient was involved in a

blasting injury. A metallic fragment entered the eye
approximately 2–3 mm posterior to the limbus and
lodged in the crystalline lens. The primary wound was
closed. A continuous curvilinear capsulorhexis was
fashioned and the foreign body was extracted through
an enlarged scleral tunnel incision. A pars plana
lensectomy and vitrectomy were performed. During the
vitrectomy, a retinal dialysis at the foreign body entry
site was discovered and repaired.
cataract surgery is performed, conventional Thus, if the risk of infection is small, inflamma-
phacoemulsification can typically be performed tion is limited, ILFB composition is acceptable,
with forceps removal of the foreign body.25 Small and cataract formation is not visually significant,
intraocular foreign bodies may resorb spontane- cautious observation is a viable option for the
ously, become encapsulated, lose magnetic prop- ILFB. However, if the ILFB is ferromagnetic,
erties and become radiolucent to X-rays. Such serial electroretinograms (ERG) should be per-
intralenticular foreign bodies can be tolerated for formed every 2–3 months to monitor for sidero-
years without surgical intervention.26 Case sis bulbi. 30,31 This feared sequela of a ferromagnetic
reports in the literature include an 18-year-old intralenticular foreign body is characterized by
male with an intralenticular foreign body and iris heterochromia, mydriasis, cataract, chronic
20/20 visual acuity 13 years after injury,27 a 61- uveitis, secondary glaucoma, retinal pigmentary
year-old male with 20/25 vision 23 years follow- degeneration, and optic disc swelling. ERG
ing injury,28 and a 58-year-old male who retained changes noted in siderosis include a large a wave
good vision without siderosis for 40 years.29 It is and normal b wave early in the course with
thought that small wounds of the anterior lens diminished (or possibly extinguished) b wave
capsule can self-seal and re-epithelialize allow- amplitude later in the course. Siderosis bulbi is
ing the foreign body to remain sequestered. discussed further in Chapter 13.
186
CASE EXAMPLES
Case report: intralenticular foreign body (Figure 12.8)

A 23-year-old male was seen in the emergency room nificant for an isolated, metallic, intralenticular foreign
complaining of a foreign body sensation in the left body (B). Given the patient’s excellent vision and lack
eye. A piece of metal had hit him in the face 3 days of infection, siderosis bulbi, or cataract, observation
prior to presentation. He had been hammering was chosen. He received oral antibiotics, topical ste-
metal on metal without protective eyewear. His roids and topical antibiotics initially and was then
initial examination was significant for a visual acuity followed with serial examinations. He was lost to
of 20/20, a normal intraocular pressure, a self-sealed follow-up but returned 6 weeks after his injury for a
corneal laceration, minimal cell and flare, an anterior baseline ERG. The ERG revealed a large a wave con-
capsular disruption (white arrow, A), and an intralen- sistent with early siderosis. The rod and cone ERG
ticular foreign body. The anterior chamber was deep responses were also increased in amplitude and pro-
and the corneal wound was negative by Seidel longed. In addition, the patient now complained of
testing. No foreign bodies were noted in the vitre- decreasing vision and was noted to have developed
ous. An ultrasound and an orbital CT scan were sig- a traumatic subcapsular cataract (C). Given his ERG
A B
Included
on DVD
C D
187
Ocular trauma
Case report: intralenticular foreign body (cont’d)

findings and the developing cataract, he underwent lens. The patient had a final visual acuity of 20/20
removal of the metallic foreign body with forceps and tolerated the procedure well without further
(D), phacoemulsification of the crystalline lens, complications.
and implantation of a posterior chamber intraocular
Posterior segment foreign bodies Timing of IOFB removal remains controversial.

Posterior segment foreign bodies represent the A posterior segment IOFB is generally considered
vast majority of IOFB and necessitate consulta- a surgical emergency. Immediate removal is thought
tion with a vitreoretinal specialist for defi nitive to reduce the incidence of endophthalmitis. The
management. Surgical intervention of posterior removal of posterior intraocular foreign bodies
segment IOFB has changed significantly with often requires a broad range of vitreoretinal tech-
the advent of closed vitrectomy. Although niques. Typical steps include stabilization of the
several studies have shown no difference in visual entry wound, pars plana lens extraction, stabiliza-
outcome using an external electromagnet (EEM) tion and repair of the retina, and forceps or mag-
versus pars plana vitrectomy (PPV), 32,33 refi ned netic removal of the foreign body. Scleral buckling
PPV techniques allow excellent control of for- is often advantageous as these cases are at a high
eign bodies and have shown a propensity for risk for the development of proliferative vitreore-
improved visual outcomes and diminished rates tinopathy (PVR). While the use of intravitreal
of endophthalmitis.34 antibiotics is controversial, the authors advocate
their use when conditions permit.
CASE EXAMPLES
Case report: intraocular foreign body (Figure 12.9)

A 30-year-old male was hammering metal on metal examination, visual acuity was 20/20 OD and 20/70
when he felt something strike his left eye. He had OS. There was no relative afferent pupillary defect
immediate mild pain and mildly decreased vision. He and intraocular pressures were 22 and 23 in the right
presented to the emergency room for treatment. On and left eye, respectively. Slit lamp examination of
A B
188
Case report: intraocular foreign body (cont’d)

the anterior segment was notable for the absence of to the fovea just inferior to the superotemporal vas-
obvious corneal lacerations or transillumination cular arcade (B). B-scan ultrasound revealed only the
defects of the iris or lens capsule. A suspicious area single IOFB visualized on dilated fundus exam (C).
was seen in the temporal sclera but was obscured The eye was covered with a shield and the patient
by focal conjunctival edema and chemosis. A small was admitted for I.V. antibiotics and surgery. A pars
amount of vitreous hemorrhage was seen on the plana vitrectomy was performed and the IOFB was
surface of the posterior capsule (A). Dilated fundus removed using an intraocular magnet. Three weeks
exam through a mild amount of vitreous hemor- following surgery, the retina was attached and the
rhage revealed a triangular-shaped metallic frag- impact site was clearly visible (D). Visual acuity was
ment embedded in the retina superior and temporal 20/200.
C D
COMPLICATIONS AND OUTCOMES cephalosporins demonstrate therapeutic concen-

trations in the vitreous. Gatifloxacin has been
Endophthalmitis is a devastating, yet common shown to achieve excellent therapeutic levels in
complication of IOFB. The reported incidence of the vitreous when administered systemically. 37
endophthalmitis following an IOFB varies widely, Vancomycin has also been shown to reach ade-
occurring in 7% 35 to 48% 36 of eyes. The risk of quate levels in eyes that are inflamed or in the
endophthalmitis is related to the mode of injury postoperative period. 38 A typical combination
and the ‘dirtiness’ of the IOFB. Intraocular regimen of an intravenous third generation
organic material and grossly dirty metallic objects cephalosporin (typically ceftazidime) and vanco-
have a very high risk of subsequent endophthal- mycin is generally given while the patient is hos-
mitis. In cases where the object is felt to be pitalized. These can be followed by an outpatient
‘clean,’ the use of prophylactic antibiotics remains course of an oral fluoroquinolone. Intraocular
controversial. Systemic antibiotics are also rou- antibiotics may also be administered at the time
tinely used, although not fully supported in the of surgery. Vancomycin (1 mg in 0.1 cc) and
literature. When selecting systemic antibiotics, a ceftazidime (2.25 mg in 0.1 cc) are well
specific goal of achieving adequate vitreous levels tolerated intravitreally and are commonly admin-
is vital. Fluoroquinolones and third generation istered prophylactically at the time of IOFB
189
Ocular trauma
removal. Broad-spectrum topical antibiotics are macular scarring, proliferative vitreoretinopathy

recommended postoperatively. and traumatic optic neuropathy are common
Beyond the direct injury inflicted by an IOFB, posterior segment causes of poor outcomes.
chemical toxicity is often a prime concern depend- Multiple reconstructive surgeries may be needed.
ing on the foreign body’s composition. Copper Visual acuity outcomes following an IOFB vary
foreign bodies are of paramount concern given the widely in published reports, but there is a clear
risk of acute chalcosis: a fulminate, sterile inflam- trend towards improved visual outcomes with
matory reaction that mimics infectious endophthal- modern surgical techniques, improved localiza-
mitis. A more benign form of chronic chalcosis can tion with computed tomography, and improved
also occur later in the disease process, typically antibiotic selection and usage in the last decade.
causing a ‘sunflower’ cataract and a green discolor- Multiple variables are associated with a poor
ation of the iris. Ferromagnetic foreign bodies can visual prognosis. These include poor preoperative
cause siderosis, a chronic deposition of iron that visual acuity, 39 relative afferent pupillary defect, 8
leads to iris heterochromia, cataract, and progres- and a large foreign body.4,6 Good visual acuity
sive pigmentary retinal degeneration. Siderosis and results are often associated with an anterior loca-
chalcosis are discussed further in Chapter 13. tion of the foreign body (anterior to the posterior
Concomitant injury to the eye is a common cause lens capsule) and minimal surrounding tissue
of poor visual outcome. Central corneal wounds injury (vitreous hemorrhage, retinal detachment,
may necessitate delayed penetrating keratoplasty. etc.). A fi nal visual acuity of ≥ 20/40 is seen in
Secondary glaucoma as well as iris and ciliary approximately 30–70% of cases.
body injury are common. Retinal detachment,
CASE EXAMPLES
Case report: intraocular foreign body (Figures 12.10)

A 38-year-old male was grinding metal wire without at which time a thorough pars plana vitrectomy was
eye protection when he felt something strike his performed to remove any vitreous traction. The
right eye. He reported immediate pain and decreased large foreign body was then carefully removed using
vision in the right eye. Initial visual acuity was 20/70 forceps (B) and the corneal wound was closed with
and 20/20 in the right and left eye respectively. 10-0 nylon sutures. Prophylactic endolaser and cryo-
Examination of the left eye was entirely normal. therapy were placed in the area of retinal disruption
Intraocular pressure measurement was deferred until (C). Gross examination of the foreign body revealed
Included
on DVD a screening slit lamp examination was performed. thin gauge wire approximately 2 cm in length (D).
An intraocular foreign body was readily visible (A). Postoperatively, the patient did well. A small corneal
The foreign body entered the inferotemporal cornea, scar and early posterior subcapsular cataract are
pierced the inferotemporal iris, entered the retina seen at a follow-up visit 2 months after surgery (E,
just posterior to the pars plana, and came to rest in just prior to suture removal). The retina remained flat
a subretinal location at the equator. A surprising lack with extensive chorioretinal scarring in the area of
of hemorrhage allowed an excellent view of the pos- retinal laser (F; white arrow denotes the anterior
terior segment. The patient was admitted and given extent of the initial IOFB position). Visual acuity was
I.V. antibiotics, tetanus prophylaxis, and topical anti- 20/30 5 months after surgery.
biotics. Surgery was undertaken several hours later
190
Case report: intraocular foreign body (cont’d)
A B
C D
E F
191
Ocular trauma
SUMMARY 7. Tomic Z, Pavlovic S, Latinovic S. Surgical treatment of

penetrating ocular injuries with retained intraocular foreign
bodies. Eur J Ophthalmol 1996;6:322–326.
1. IOFB is a harrowing diagnosis for the patient
8. De Souza S, Howcroft MJ. Management of posterior segment
and ophthalmologist. intraocular foreign bodies: 14 years’ experience. Can J
2. IOFB most commonly occurs in young men Ophthalmol 1999;34:23–29.
hammering metal on metal in the absence of 9. Dannenberg AL, Parver LM, Brechner RJ, Khoo L. Penetrating
protective eyewear. eye injuries in the workplace: the National Eye Trauma System
3. Careful history taking and examination are a Registry. Arch Ophthalmol 1992;110:843–848.
10. Armstrong MFJ. A review of intraocular foreign body injuries
vital portion of the workup and can secure the
and complications in N. Ireland from 1978–1986. International
diagnosis in some instances, but computed Ophthalmology 1988;12:113–117.
tomography or ultrasound are often necessary 11. Behrens-Baumann W, Praetorius G. Intraocular foreign bodies,
to confi rm the diagnosis and rule out multiple 297 consecutive cases. Ophthalmologica 1989;198:84–88.
foreign bodies. 12. Punnonen E, Laatikainen L. Prognosis of perforating eye
4. Surgical removal of an IOFB is determined by injuries with intraocular foreign bodies. Acta Ophthalmol
1989;67:483–491.
the fi nal resting place of the foreign body as
13. Greven CM, Engelbrecht NE, Slusher MM, Nagy SS. Intraocular
well as concomitant ocular injuries. foreign bodies: management, prognostic factors, and visual
5. Metallic intralenticular foreign bodies must outcomes. Ophthalmology 2000;107:608–612.
be followed serially with electrophysiologic 14. Bryden FM, Pyott AA, Bailey M, McGhee CNJ. Real time
testing if observation is elected. ultrasound in the assessment of intraocular foreign body.
6. Posterior segment IOFB requires consultation Eye 1990;4:727–731.
15. Bray LC, Griffiths PG. The value of plain radiography in
with a vitreoretinal specialist for defi nitive
suspected intraocular foreign body. Eye 1991;5:751–754.
management. 16. Dass AB, Ferrone PJ, Chu YR, et al. Sensitivity of spiral
computed tomography scanning for detecting intraocular
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blindness after MR study. Am J Neuroradiology 1986;7: 1990;97:1532–1538.
243–245. 34. Mester V, Kuhn F. Ferrous intraocular foreign bodies retained
24. Essex RW, Yi Q, Charles PG, Allen PJ. Post-traumatic in the posterior segment: management options and results.
endophthalmitis. Ophthalmology 2004;111:2015–2022. Int Ophthalmol 1998;22:355–62.
25. Arora R, Sanga L, Kumar M, Taneja M. Intralenticular foreign 35. Mieler WF, Ellis MK, Williams DF, Han DP. Retained intraocular
bodies: report of eight cases and review of management. foreign bodies and endophthalmitis. Ophthalmology
Indian J Ophthalmol 2000;48:119–122. 1990;97:1532–1538.
26. Lee LL, Briner AM. Intralenticular metallic foreign body. 36. Kazokoglu H, Saatci O. Intraocular foreign bodies: results of 27
Australian NZ J Ophthalmol 1996;24:361–363. cases. Ann Ophthalmol 1990;22:373–376.
27. Keeney AH. Intralenticular foreign bodies. Arch Ophthalmol 37. Hariprasad SM, Mieler WF, Holz ER. Vitreous and aqueous
1971;86(5):499–501. penetration of orally administered gatifloxacin in humans.
28. Macken PL, Boyd SR, Feldman F. Intralenticular foreign bodies: Arch Ophthalmol 2003;121:345–350.
case reports and surgical review. Ophthalmic Surg 1995;26(3): 38. Meredith TA, Aguilar HE, Shaarawy A, et al. Vancomycin levels
250–252. in the vitreous cavity after intravenous administration. Am J
29. Cazabon S, Dabbs TR. Intralenticular metallic foreign body. Ophthalmol 1995;119:774–778.
J Cataract Refract Surg 2002;28:2233–2234. 39. Jonas JB, Knorr HL, Budde WM. Prognostic factors in ocular
30. O’Duffy D, Salmon JF. Siderosis bulbi resulting from injuries caused by intraocular or retrobulbar foreign bodies.
an intralenticular foreign body. Am J Ophthalmol Ophthalmology 2000;107:823–828.
1999;127(2):218–219.
31. Sneed SR, Weingeist TA. Management of siderosis bulbi due
to a retained iron-containing intraocular foreign body.
Ophthalmology 1990;97(3):375–379.
193
13
Delayed complications of
ocular injury
James T. Banta
INTRODUCTION TRAUMATIC CATARACT
Ocular trauma, as illustrated in the previous A cataract may develop any time following a
chapters, is a diverse spectrum of disease pro- traumatic injury. The timeframe depends pri-
cesses affecting all portions of the eye. Most marily on the mechanism of trauma. Direct
injuries lead to a rapid onset of symptoms and injury to the lens capsule often leads to immedi-
diagnostic dilemmas are fairly unusual once ate formation of cataract, whereas mature cata-
a familiarity with the various conditions is racts can present decades after a contusive
obtained. It is important to note, however, that injury. It is important to elucidate a history of
multiple pathologic conditions do not present trauma when planning cataract surgery since
acutely. Many can be delayed by days (traumatic antecedent trauma predisposes to zonular injury
iritis) to months (traumatic cataract) to years and intraoperative complications. Symptoms
(angle recession glaucoma). are usually limited to diminished vision. Signs
In this chapter, we will describe ocular com- include phacodonesis, iridodonesis, lens sublux-
plications of ocular trauma that are not necessar- ation/dislocation, vitreous prolapse or a monoc-
ily present on initial examination and which ular mature cataract. Traumatic cataract is
require prolonged follow-up. These entities covered in detail in Chapter 7.
range from self-limited to vision-threatening and
require diligence on the part of the physician to DELAYED TRAUMA-RELATED
correctly diagnose and treat. Diagnoses covered GLAUCOMA
in prior chapters will be mentioned briefly and
cross-referenced to the chapter containing a Glaucoma can occur via multiple mechanisms
detailed description. following ocular trauma. Some forms of glau-
coma may occur months to years following the
TRAUMATIC IRITIS inciting injury, re-emphasizing the importance
of appropriate long-term follow-up after ocular
Traumatic iritis is a very common condition trauma.
that typically occurs hours to days after a contu-
sive injury to the eye. Typically, an antecedent Angle recession glaucoma
history of ocular injury, often mild, is elucidated. Contusive ocular injury can lead to a rapid equa-
Common presenting symptoms include photo- torial expansion of the eye. One manifestation
phobia, blurry vision, and pain. Examination of this injury type is a traumatic separation of
fi ndings include conjunctival injection and an the longitudinal and circular fibers of the ciliary
anterior chamber cellular response. Treatment body. Angle recession has a characteristic gonio-
involves cycloplegia plus or minus steroid drops. scopic appearance and should be specifically
Traumatic iritis is covered in detail in Chapter 6. ruled out after any substantial contusive eye
195
Ocular trauma
injury. Angle recession is covered in detail in degree of clinical suspicion. A thorough history
Chapter 6. is of the utmost importance since the inciting
injury can be fairly remote.
Vitreous hemorrhage-induced glaucoma
Following traumatic vitreous hemorrhage, par- Lens-induced glaucoma
ticularly in patients with disruption of the Trauma to the crystalline lens can cause glau-
anterior hyaloid face and zonular apparatus, red coma by a variety of open and closed angle
blood cells (RBC) and RBC breakdown products mechanisms. The primary clinical entities
can freely fi lter into the anterior chamber and include:
obstruct the trabecular meshwork. Three dis- 1. Phacolytic glaucoma. Elevated IOP caused by
tinct entities have been described depending on leakage of lens proteins through the intact
the level of RBC breakdown that has occurred: capsule of a hypermature cataract.
1. Ghost cell glaucoma. RBCs undergo a step- 2. Phacomorphic glaucoma. Elevated IOP caused
wise degradation as they remain in the vitre- by angle closure induced by a mature or
ous cavity. Dehemoglobinized cells are more rapidly evolving traumatic cataract.
rigid and spherical than regular RBCs and 3. Lens particle glaucoma. Elevated IOP caused
mechanically block the trabecular meshwork by mechanical blockage of the trabecular
when introduced to the anterior chamber. meshwork by liberated lens particles following
Khaki-colored cells can often be seen circulat- trauma.
ing in the anterior chamber and sometimes 4. Phacoanaphylactic glaucoma. Elevated IOP
layer out as a pseudo-hypopyon. caused by profound granulomatous inflamma-
2. Hemolytic glaucoma. Further degradation of tory response to liberated lens particles.
RBCs leaves cellular debris, free hemoglobin, Lens-induced glaucoma is covered in detail in
and macrophages laden with breakdown prod- Chapter 7.
ucts to mechanically obstruct the trabecular
meshwork.
3. Hemosiderotic glaucoma. Iron freed during RETINAL DETACHMENT
the breakdown of RBCs can be toxic to the
endothelium lining the trabecular meshwork Retinal detachment is the fi nal common pathway
months to years after vitreous hemorrhage. for an array of trauma-induced peripheral retinal
This toxicity can lead to sclerosis and mal- injuries. Vitreoretinal attachments are much
function of aqueous egress from the eye with stronger in young patients, the demographic
subsequently elevated intraocular pressure. representing most ocular traumas. When
Treatment for each of these forms of glaucoma these attachments are traumatically disrupted, a
begins with standard medical therapy to slow variety of injuries occur including:
aqueous production and facilitate outflow. If 1. retinal dialysis
these measures are unsuccessful, as they 2. giant retinal tear
frequently are, surgical intervention with pars 3. horseshoe tear
plana vitrectomy and anterior chamber washout 4. pars plana tear
is frequently necessary. The diagnosis of these 5. necrotic retinal break
very rare forms of glaucoma requires a high 6. vitreous base avulsion.
196
Delayed complications of ocular injury
Careful peripheral retinal examination is vital clinical evaluation is critical for the diagnosis of
following ocular injury. If a view to the posterior an intraocular foreign body given its propensity
segment is obstructed or scleral depression is not for infection and toxicity. Most IOFB are metal-
possible due to concomitant injuries, ultrasound lic and occur in young males hammering metal
can be used to monitor the status of the retina. on metal or grinding. The composition of an
Traumatic retinal detachment is covered in IOFB determines its toxicity to the eye (Table
detail in Chapter 8. 13.1). Precious metals such as gold and platinum
are well tolerated in the posterior segment.
METALLOSIS BULBI Foreign bodies containing iron or copper are
common and can lead to severe ocular toxicity
Retained intraocular foreign body (IOFB) occurs and potential blindness.
in 5–40% of all open globe injuries. Careful
Table 13.1 Intraocular foreign body composition and subsequent toxicity
Substances Inflammatory and toxic reactions
Anterior chamber Posterior chamber

Stone, clay, sand Mild, though chronic uveitis not Mild, though chronic uveitis not
uncommon uncommon
Concrete Mild, may be recurrent Not reported
Coal Mild Mild, may be recurrent
Carbon Mild Mild
Gunpowder, cordite None to mild None to mild
Glass, quartz, porcelain Mild chronic uveitis possible if Usually mild

Non-metallic
uveal tract involved
Thermo/plastics Similar to glass Similiar to glass

(poly-methyl
Inert
methacrylate,
-ethylene and -amides)
Thermoplastics Severe inflammation Severe inflammation

(bakelite, casein)
Rubber None to mild Not reported
Talc Chronic inflammation Chronic inflammation
Silk None to mild None to mild
Gold and tantalum None to mild Retinal degeneration if chronic

Precious
metals
Silver and None to mild Retinal degeneration if chronic

platinum
197
Ocular trauma
Table 13.1 Intraocular foreign body composition and subsequent toxicity—cont’d
Substances Inflammatory and toxic reactions

Anterior chamber Posterior chamber
Lead None to mild Mild to severe, may have retinal
degeneration
Nickel Purulent Purulent, eventually

encapsulated
Aluminum Varied, iridocyclitis and corneal Mild iridocyclitis and vitreal

opacification possible opacities
Irritative
Metallic
Mercury Purulent leading to enucleation Purulent leading to enucleation
Copper (pure) Purulent leading to enucleation, Purulent leading to enucleation

less toxic in lens
Brass and bronze Chalcosis: deposits in Chalcosis: framework of vitreous

(<85% copper) Descemet’s, lens capsule and and surface of retina
zonules
Iron Six reactions: (1) none (2) delayed inflammation (3) spontaneous
expulsion (4) dissolved (5) sympathetic (6) siderosis
Cotton fibers (surgically) None to mild None to mild

Vegetable
Wood Mild to severe or endophthalmitis Severe or endophthalmitis

Organized
Straw, grain and grass Sterile: no reaction, non-sterile: purulent or infection

Animal
Bone None to mild and may absorb
Cilia None to mild, delayed inflammation or cysts
Siderosis bulbi 1. Generally, smaller foreign bodies are better

Sidersosis bulbi, also referred to as ocular tolerated and can sometimes be resorbed
siderosis, refers to the toxic effects on the eye spontaneously.1
from a retained iron-containing IOFB. Although 2. Fibrotic encapsulation can limit the disper-
similar in some respects, ocular hemosiderosis sion of toxic iron breakdown products, delay-
refers to the toxic effects on the eye from ing but not necessarily preventing the onset of
iron released following a massive intraocular siderosis.
hemorrhage. 3. In general, anterior iron-containing IOFB are
The pathophysiology of siderosis bulbi is not better tolerated than equivalent posterior
completely understood. The size, amount of encap- segment foreign bodies, although siderosis can
sulation, and location of an iron-containing IOFB develop even if the IOFB is within the sub-
can lead to a highly variable clinical course: stance of the crystalline lens.
198
4. Rarely, iron-containing IOFB can be present

for many years without toxicity.
Histologic examination of eyes with siderosis
reveals deposition of iron breakdown products
throughout the tissues of the eye. Siderosomes
are discrete intracellular organelles that contain
iron breakdown products and are observed in
cells with significant degenerative changes.2,3
Clinical fi ndings typically present several
months to years after injury, but have been
reported as soon as 18 days after injury.4 Classic
fi ndings include:
1. iris heterochromia (involved iris is darker, Figure 13.1 Rust-colored deposits are seen in a
subcapsular location in this patient with ocular
most evident in patients with lightly colored
siderosis.
irides)
Figure 13.2 Diffusely supernormal responses are seen in the left eye of a young man who was being serially
followed for a metallic intralenticular foreign body. The findings were consistent with the acute phase of siderosis
and prompted surgical extraction of the foreign body in conjunction with cataract extraction.
199
Ocular trauma
2. poorly reactive, enlarged pupil evaluation is mandatory. Siderosis initially causes

3. anterior subcapsular lens deposits (Figure an increase in the a wave (Figure 13.2) followed
13.1) by a progressive decline in the b wave later in the
4. dark corneal endothelium deposits disease (see Case report). In very late stages
5. optic disc edema with angiographic leakage the ERG is extinguished. Once ERG changes
6. pigmentary retinopathy; typically a late develop, removal of the IOFB should be per-
fi nding. formed expediently as electrophysiologic changes
In the uncommon instance observation for an are sometimes reversible.5
IOFB is elected, serial electroretinogram (ERG)
CASE EXAMPLES
Case report: siderosis secondary to IOFB (Figure 13.3)

A 24-year-old male was hammering metal on metal attention. Two months later, he presented with a
without eye protection when he felt something progressive decline in vision of the left eye. Visual
Included
on DVD
strike his left eye. Despite a foreign body sensation acuity was 20/200 OS with an afferent pupillary
and decreased vision, he did not seek medical defect. Anterior segment evaluation was normal.
A B
D
C
200
Case report: siderosis secondary to IOFB (cont’d)

Dilated fundus exam revealed a single metallic intra- diagnosis of siderosis bulbi was made. The patient
ocular foreign body in the superonasal periphery underwent uneventful par plana vitrectomy and
surrounded by extensive pigmentary alterations (A). removal of the intraocular foreign body. (D) The
B-scan ultrasound revealed only the single intra- foreign body was removed by intraocular forceps
ocular foreign body (B). An electroretinogram was through a sclerotomy incision. Visual acuity remained
obtained and revealed severe, diffuse depression of 20/200 postoperatively.
both photopic and scotopic examinations (C). The
Chalcosis 1. sunflower cataract

Retained copper-containing IOFB is an uncom- 2. iris heterochromia (typically a greenish dis-
mon clinical entity. Common sources of injury coloration of the affected iris)
with copper include explosions (bullet casings, 3. deposits on the retinal surface
mines, or grenades) and industrial work with 4. free copper particles in the aqueous or
copper alloys. The most common copper vitreous
alloys are brass and bronze, both of which 5. Descemet’s membrane deposits forming a
typically contain less than 85% copper. Intraocu- peripheral corneal ring (Kayser–Fleischer).
lar copper foreign bodies show a wide range The clinical course of chronic chalcosis is vari-
of fi ndings ranging from an acute fulminant, able, but typically indolent. ERG changes are
endophthalmitis-like picture to an indolent typically absent or minimal.8 Removal of the
deposition of copper in various ocular basement foreign body should be undertaken if visual com-
membranes. promise is evident.
Acute chalcosis is typically seen with foreign
bodies containing more than 85% copper.6 It is SYMPATHETIC OPHTHALMIA
characterized by a profound inflammatory
response that leads to destruction of intraocular Sympathetic ophthalmia is one of the least
contents within a short period of time. The only common yet most feared complications of ocular
treatment is expedient removal of the offending trauma. It is a bilateral granulomatous uveitis
foreign body and the outcomes are typically that occurs after injury to the eye, most com-
poor. It is important to note that this reaction monly following open globe injury but also
does not occur universally, even with pure copper known to occur after intraocular surgery. 9 The
foreign bodies.7 pathophysiology of the disease process, particu-
Although variable, classic teaching states that larly the antigen that elicits the inflammation, is
chronic chalcosis occurs with IOFB containing debated; but it appears that upon traumatic
less than 85% copper.6 The inflammatory injury, uveal antigens are exposed in a manner
response is less severe and may be minimal. The that elicits a delayed autoimmune response.
primary mechanism of toxicity is deposition of The exciting, or injured eye, becomes inflamed as
copper in various membranes within the eye. does the sympathizing, or previously normal, eye.
Classic ocular fi ndings include: A genetic predisposition may be a factor as indi-
201
Ocular trauma
cated by the increased prevalence of HLA-A11 strategies. Enucleation of a severely injured eye
in sympathetic ophthalmia patients.10 is thought to prevent sympathetic ophthalmia if
Sympathetic ophthalmia is rare. The incidence performed within 10–14 days of injury. However,
following open globe injury is approximately with current medical and surgical care, improved
0.2%11 to 0.5%.12 The time to onset following visual outcomes are being seen following severe
injury is highly variable, typically ranging ocular trauma. Enucleation is typically reserved
from 2 weeks to 6 months with most cases for eyes with no hope of visual recovery and
presenting within 3 months of injury. However, prominent intraocular disorganization. A candid
it has been reported to occur as early as 10 days discussion with the patient regarding the risks of
and as late as many decades following the sympathetic ophthalmia is mandatory if enucle-
inciting event. ation is being considered following open globe
The clinical onset is often insidious over days repair.
to weeks. Mild, vague complaints are often Once active sympathetic ophthalmia has been
encountered early in the disease course. Mild diagnosed, treatment consists primarily of immu-
pain, photophobia, and mildly decreased vision nosuppressive agents. The use of enucleation to
are common presenting symptoms. The symp- remove the exciting eye is controversial and
toms predominate in the sympathizing eye since unlikely of any benefit.13 In some circumstances,
the exciting eye often has poor vision and mild, after the disease has progressed, the exciting eye
chronic discomfort. This reinforces the need for can maintain better visual acuity than the sym-
careful examination of the uninjured eye follow- pathizing eye. Current medical regimens rely
ing an open globe injury, particularly if the heavily on steroids in high doses with long,
injured eye has protracted inflammation and gradual tapers. Steroid sparing agents such as
pain following surgical repair. cyclosporine, azathioprine, chlorambucil, and
The clinical appearance of sympathetic oph- methotrexate have all been used with success.
thalmia is variable, but typically involves a granu- Although the exact regimen is controversial,
lomatous panuveitis with a prominent vitritis and aggressive therapy in a timely manner is vital to
characteristic changes of the posterior pole. clinical success. Long-term follow-up is required
Mutton-fat keratic precipitates are often seen on as long periods of remission may punctuate epi-
the corneal endothelial surface in the active phase sodes of activity.
of the disease. The choroidal lesions are often Outcomes in sympathetic ophthalmia prior to
multifocal, placoid, and cream-colored. The cho- the routine use of high dose steroids were uni-
roidal lesions correspond to Dalen–Fuchs nodules, formly poor. Refi nements in medical therapy
a histologic diagnosis. Optic nerve hyperemia have improved the visual outcomes significantly.
and swelling are sometimes present. Fluorescein A review of 32 sympathetic ophthalmia cases
angiography reveals multiple hyperfluorescent treated with systemic steroids showed 50%
sites that leak late in the angiogram. recovered vision of 20/40 or better; however,
Treatment of sympathetic ophthalmia can be 31% had a fi nal visual acuity less than
broken up into preventative and active treatment 20/200.14
202
CASE EXAMPLES
Case report: sympathetic ophthalmia (Figure 13.4)

A 33-year-old female was forcefully struck in the right revealed keratic precipitates, anterior chamber cell
eye with a fist and experienced immediate and pro- and flare, and 360 degrees of posterior synechiae (B).
found loss of vision. She was evaluated by an oph- Dilated fundus examination of the left eye revealed
thalmologist who was suspicious for a ruptured optic nerve swelling and hyperemia. Multifocal
globe. The patient was taken to the operating room cream-colored choroidal lesions and serous retinal
and a full-thickness 8 mm scleral wound was closed detachments were present throughout the posterior
uneventfully. The patient failed to return for follow- pole (C). Ocular coherence tomography further
up. One month after the surgical repair, the patient delineated the multifocal serous detachments (D).
presented to our ocular emergency room with com- The patient was admitted on multiple occasions for
plaints of profound decreased vision and pain for 3 intravenous steroids and was discharged on oral ste-
days in the left eye. Ophthalmic examination revealed roids. Due to a poor social situation and struggles
a visual acuity of light perception in the right eye and with drug dependence, the patient failed to return
20/200 in the left eye. Slit lamp examination of the for most of her follow-up appointments and dem-
right eye revealed a shallow but formed anterior onstrated poor compliance throughout her treat-
chamber with a small amount of residual hyphema ment course. One year after her initial presentation,
and a dense cataract precluding a view of the pos- vision remained hand motions in the right eye and
terior pole (A). Slit lamp examination of the left eye 20/200 in the left eye.
A B
C D
203
Ocular trauma
CHOROIDAL NEOVASCULARIZATION ocular disruption imparted by the inciting injury

ASSOCIATED WITH CHOROIDAL and subsequent surgical repair. A high index of
RUPTURE suspicion and a low threshold for intervention
are necessary. The presence of a hypopyon and
Choroidal ruptures occur after contusive trauma increasing membranous vitreous opacities (by
and appear as curvilinear, crescent-shaped areas clinical examination or ultrasound if posterior
concentric to the optic disc. The major cause of viewing is compromised) are classic fi ndings of
poor vision resulting from choroidal rupture, endophthalmitis and should prompt emergent
second to a rupture involving the fovea, is late treatment.
development of a choroidal neovascular mem- The diagnosis of endophthalmitis is clinical, as
brane (CNVM). Metamorphopsia and decreased cultures of intraocular contents can be negative.
vision typically occur if the CNVM occurs However, it is vital to obtain cultures and sensi-
within the macula. Clinical examination often tivities to further guide antibiotic choices and
reveals a greenish-gray subretinal lesion that may identify potential patterns of emerging antibiotic
be associated with hemorrhage or subretinal resistance. The spectrum of isolated organisms
fluid. Fluorescein angiography is used to confi rm following an open globe injury is unique. A
the diagnosis. particularly high incidence of Bacillus species
CNVM associated with choroidal rupture is and polymicrobial infections are encountered.
covered in detail in Chapter 8. Gram positive organisms make up a majority of
infections20–22 with Staphylococcus epidermidis,
Bacillus cereus, and Streptococcus species being
TRAUMATIC ENDOPHTHALMITIS the most common gram positive isolates.22 Gram
negative organisms (particularly Pseudomonas
Traumatic endophthalmitis is a feared complica- species) and fi lamentous fungi are seen with less
tion of open globe injury. The incidence of frequency. Bacillus species have a particularly
this potentially devastating complication ranges fulminate course with rapid onset and a dismal
widely in published reports. In years past, visual prognosis and should be suspected if endo-
reported rates have been as high as 30% follow- phthalmitis develops within the fi rst few days
ing open globe injury.15 However, more recent following the inciting injury.
studies report rates less than 10%, typically 4– Two primary choices in treatment exist once
7%.16–18 The presence of an intraocular foreign the diagnosis is made:
body increases the rate two- to threefold. 1. vitreous aspiration for culture with intravit-
Risk factors for developing endophthalmitis real injection of antibiotics
following open globe injury include: 2. pars plana vitrectomy with intravitreal injec-
1. intraocular foreign body17 tion of antibiotics.
2. violation of lens capsule17–19 The preferred treatment strategy depends on
3. contaminated wound17 multiple variables including the status of the lens
4. delay in primary repair.7 and posterior segment. Chapter 14 discusses in
Most patients with traumatic endophthalmitis further detail the controversy surrounding the
present with increasing eye pain following open management of traumatic endophthalmitis.
globe repair. The diagnosis is often difficult The prophylactic use of antibiotics in the peri-
owing to the extensive inflammation and intraoperative period of an open globe injury is some-
204
what controversial, although nearly universally versy surrounding the prophylactic treatment
utilized. Some studies have shown a decline in of post-traumatic endophthalmitis in further
post-traumatic endophthalmitis rates with the detail along with authors’ recommendations for
routine use of prophylactic antibiotics.23 However, treatment.
the antibiotic selection and preferred route of The visual prognosis for post-traumatic endo-
delivery vary greatly from practitioner to practi- phthalmitis is often poor. Multiple studies have
tioner. Topical antibiotics are used in all cases shown a wide range of visual outcomes, mostly
and are often supplemented with intravenous, dependent on the virulence of the organisms
subconjunc-tival, intracameral, intravitreal or isolated. Visual acuity ≥ 20/400 was seen in
oral antibiotics. Chapter 14 discusses the contro- 22–75% of cases.17,18,21,22,24,25
CASE EXAMPLES
Case report: traumatic endophthalmitis (Figure 13.5)

A 60-year-old male slipped on the lower rungs of a A CT scan was performed to rule out an intraocular
ladder and in an effort to stabilize himself acciden- foreign body. The patient was taken to the operating
tally stabbed himself in the left eye with a sharpened room where the scleral laceration was closed
pencil he was holding. Initial examination of the left and a pars plana lensectomy and vitrectomy was
eye revealed a visual acuity of hand motions and an performed. The patient presented 5 days after
intraocular pressure of 7 (compared to 19 in the surgery with increasing pain and nausea. Visual
fellow eye). Slit lamp examination revealed an infero- acuity was bare light perception and intraocular
temporal conjunctival laceration overlying a likely pressure was 25. Slit lamp examination revealed
scleral laceration. A small hyphema was present in severe conjunctival injection, corneal edema, and a
the anterior chamber and no view of the posterior small layered hypopyon (B). A diagnosis of traumatic
pole was possible due to vitreous hemorrhage (A). endophthalmitis was made. A vitreous aspirate was
A B
205
Ocular trauma
Case report: traumatic endophthalmitis (cont’d)

obtained for culture and intravitreal antibiotics were patient, the decision was made to enucleate the
injected (vancomycin and ceftazidime). Cultures injured eye. Gross pathologic examination revealed
began growing Candida albicans 3 days after the extensive fungal involvement in the retina, vitreous,
sample was collected. Despite future intravitreal ciliary body, and anterior chamber (D). The patient
injections of amphotericin B and voriconazole along did well following enucleation with complete resolu-
with oral fluconazole, the patient deteriorated to tion of pain. Polycarbonate spectacles were pre-
bare light perception vision with severe, debilitating scribed for full-time use.
pain (C). After an extensive discussion with the
C D
CONCLUSIONS SUMMARY
It is difficult to give specifics on the appropriate 1. Red blood cell breakdown products can cause
interval for follow-up after ocular trauma because glaucoma by directly blocking the trabecular
of the immense diversity in presentation and meshwork.
severity. Follow-up must be tailored to the indi- 2. Iron- and copper-containing foreign bodies
vidual situation. The authors recommend goni- can lead to severe toxic reactions in the eye if
oscopy and dilated fundus examination in every not expediently removed.
patient with ocular trauma a month after pre- 3. Sympathetic ophthalmia is a feared complica-
sentation if the inciting injury was of significant tion of ocular trauma and often directs the
force to cause intraocular inflammation (iritis) management of the severely injured eye.
or disruption (commotio retinae). Of particular 4. The incidence of traumatic endophthalmitis
concern are high-velocity contusive injuries. has fallen since the widespread use of prophy-
Gonioscopy is performed to determine if angle lactic antibiotics in the setting of an open
recession has occurred. A dilated fundus exami- globe, although the selection and route of
nation is important to evaluate the lens for cata- antibiotic delivery remains controversial.
ract and the peripheral retina for possible tears,
dialyses, or detachments.
206
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associated with pars plana vitrectomy without antecedent
22. Affeldt JC, Flynn HW Jr., Forster RK, et al. Microbial
penetrating trauma. Retina 2001;21:146–154.
endophthalmitis resulting from ocular trauma. Ophthalmol
10. Reynard M, Shulman IA, Azen SP, Minckler DS.
1987:94:407–413.
Histocompatability antigens in sympathetic ophthalmia. Am J
23. Joosse MV, Van Tilburg CJG, Mertens DAE, et al.
Ophthalmol 1983;95:216–221.
Endophthalmitis: incidence, therapy and visual outcome
11. Liddy N, Stuart J. Sympathetic ophthalmia in Canada. Can J
in the period 1983–1992 in the Rotterdam Eye Hospital.
Ophthalmol 1972;7:157–159.
Doc Opthalmol 1992;82:115–123.
12. Holland G. About the indications and time for surgical
24. Peyman GA, Carroll CP, Raichand M. Prevention and
removal of an injured eye. Klin Monatsbl Augenheilkd
management of traumatic endophthalmitis. Ophthalmology
1964;145:732–740.
1980;87:320–324.
13. Winter FC. Sympathetic uveitis: a clinical and pathologic
25. Nobe JR, Gomez DS, Liggett P, Smith RE, Robin JB. Post-
study of the visual result. Am J Ophthalmol 1955;39:
traumatic and postoperative endophthalmitis: a comparison
340–347.
of visual outcomes. Br J Ophthalmol 1987;71:614–617.
14. Chan C, Roberge FG, Whitcup SM, Nussenblatt RB. 32 cases
of sympathetic ophthalmia, a retrospective study at the
National Eye Institute, Bethesda, Md, from 1982 to 1992.
Arch Ophthalmol 1995;113:597–600.
207
Ocular trauma controversies
Andrew C. Westfall, Matthew S. Benz
INTRODUCTION
14
Nevertheless, maintaining an ongoing discourse
on these subjects will hopefully lead to consen-
Ocular trauma remains a prevalent and largely sus agreements on the most appropriate methods
preventable cause of visual morbidity. As you of medical and surgical intervention, even if true
have read in previous chapters, traumatic injuries prospective data are unavailable. It is for these
of the globe range from simple corneal abrasions reasons that this chapter has been included, not
to complex corneoscleral lacerations. Such inju- to give defi nitive answers, but to continue the
ries are suffered by children and adults of all dialogue.
ages, in the home as well as at work and on holi-
days. While the types of eye trauma suffered by INTRAOCULAR FOREIGN
patients and the treatment concerns of clinicians BODY REMOVAL
are similar to those of years past, treatment
options and technology have undergone a tre- Intraocular foreign body (IOFB) is an uncom-
mendous evolution. Due to the unpredictable, mon type of ocular trauma but accounts for a
varied and often urgent nature of ocular trauma, large portion of the cases requiring extensive
a paucity of prospective outcomes data exists surgical intervention. The epidemiology, patho-
and controversies persist. Below, we present a physiology, evaluation and initial management of
discussion of current topics in ocular trauma, an IOFB have been thoroughly discussed in
with particular attention to controversies over Chapter 12. However, significant controversies
management. Most controversies involve differ- exist concerning the timing of posterior segment
ences in opinion on the best way to preserve IOFB removal and the most appropriate method
vision while minimizing the number of surgeries of foreign body removal, especially with mag-
and avoiding undue stress on a compromised netic intraocular foreign bodies.
eye.
The subjects discussed in this section are Timing of IOFB removal
advanced issues and are directed primarily at the Several items often dictate the timing of IOFB
sub-specialist ophthalmologist who will be inter- removal:
vening surgically. The timing and extent of initial 1. IOFB composition and toxicity
surgical intervention has long been controversial 2. the risk of infection
and most eye surgeons who deal with surgical 3. the presence or absence of a posterior vitreous
eye trauma base their methods on experience detachment (PVD)
and anecdotal information. It will be difficult to 4. the risk of suprachoroidal hemorrhage.
ever have a defi nitive answer to many of these The composition of a foreign body determines
questions given the lack of similarity from injury the potential for toxicity, inflammation, or infec-
to injury and the resultant difficulty in planning tion, thereby dictating the immediacy of surgical
and carrying out any sort of prospective study. intervention. If the foreign substance is soil,
209
Ocular trauma
vegetable matter, or copper, then few would dis- 1. Frequent clinical examinations are necessary
pute the need for immediate removal given the to detect evolving retinal tears, retinal detach-
tremendous risk of infection with organic mate- ment, ocular toxicity and infection. If a
rial and the severe toxic reactions encountered view of the posterior pole is limited by
with copper foreign bodies (see Chapter 13). vitreous hemorrhage, traumatic cataract or
With foreign bodies that have less potential for corneal opacity, then serial ultrasounds are
ocular toxicity (e.g. glass, plastic, or steel), the necessary.
issue becomes less clear. Some practitioners 2. Appropriate coverage with systemic antibiot-
advocate postponing IOFB removal until a PVD ics with proven intravitreal penetration should
can be documented by examination or ultra- be utilized.
sound, and the risk of choroidal hemorrhage is 3. If the foreign body is ferrous, serial electro-
decreased.1–4 retinograms should be performed to detect
Advocates for immediate foreign body removal signs of toxicity.4
cite the risk of intraocular infection as being 4. Vitrectomy should be performed expedi-
too high (3–17%) to wait for a PVD to occur tiously once a PVD has occurred since vitre-
without an unacceptable risk of permanent vision ous organization will occur approximately 14
loss.5–17 Theoretically, by removing the IOFB days post-injury and the risk of tractional
and using antibiotics within 24 hours of the retinal detachments will increase thereafter.
injury, it is possible to significantly reduce
the risk of infection.5,9,10 In addition, immediate Instrumentation for IOFB removal
IOFB removal limits the formation of fibrin The ability to successfully remove foreign bodies
around the IOFB, thereby facilitating removal. from the posterior segment has advanced over the
Another argument for early removal is earlier years with the progress of surgical technology.
recovery. Once a patient sustains injury from Prior to vitrectomy, an external magnetic was
an IOFB, the road to recovery can be long and used for the removal of all magnetic IOFBs.19–21
fi lled with multiple surgeries. If removal of the With external magnets, Snellen visual acuity
IOFB is possible at the time of primary closure, of 20/40 was achieved 55–60% of the time.22
healing and visual recovery can sometimes be However, most authors believe the use of magnets
expedited.18 external to the globe poses unnecessary risks
Vitreoretinal surgeons in favor of delayed IOFB to the retina, including retinal tears and detach-
removal prefer waiting for a spontaneous PVD ments, vitreous hemorrhage, cataract formation,
which frequently occurs between 10 and 14 days new contusion injuries, and retention of
after the initial injury. Waiting for a PVD is IOFBs.6,18,22,23
reasonable, particularly in young patients where With the advent of pars plana vitrectomy, it
a pre-existing PVD is unlikely and creating a became possible to use internal magnets or intra-
mechanical PVD is not always possible. Postop- ocular forceps to remove foreign bodies from the
eratively, an intact posterior hyaloid face increases posterior segment under direct visualization
the risk for proliferative vitreoretinopathy and (Figure 14.1).8,12 Although a defi nitive study has Included
on DVD
subsequent tractional retinal detachment. not been performed which demonstrates the
If delayed IOFB removal or observation is superiority of vitrectomy techniques versus the
chosen over immediate removal, several items use of an external magnet, it is clear that
must be assured: ancillary damage such as cataracts, vitreous
210
A B C
Figure 14.1 Closed vitrectomy techniques allow removal of posterior segment foreign bodies in a controlled
fashion and under direct visualization. A pars plana vitrectomy is initially performed to clear the vitreous cavity
and locate the foreign body (A). The foreign body is then brought into the anterior vitreous cavity with an
intraocular magnet (B) before being transferred to intraocular forceps and removed through a sclerotomy (C).
(After Recchia FM, Aaberg Jr T, Sternberg Jr P. Trauma: Principles and techniques of treatment. In: Ryan SJ, ed.
Retina, 4th edn. Philadelphia: Elsevier Mosby; 2004:2391, with permission from Elsevier.)
hemorrhage, retinal tears and detachments can instrumentation, perfluorocarbon can now be
be prevented when using direct visualization used when non-metallic foreign bodies are
possible only with closed vitrectomy tech- present. This allows ‘floating’ of objects off the
niques.23 Also, vitrectomy allows for removal of retinal surface. The suspended object can then
encapsulated foreign bodies and intraretinal be grasped with intraocular forceps and subse-
foreign bodies which may not always be possible quently removed without making contact with
with the use of external magnets.6 Theoretically, the retinal surface.20,21
one can also decrease the risk of endophthalmitis
by reduction or removal of the inciting organisms PROPHYLACTIC SURGICAL TECHNIQUES
from the vitreous cavity.5 Despite the more con- IN THE OPEN GLOBE
trolled extraction of foreign bodies with vitrec-
tomy, fi nal visual acuity (60% with > 20/40 If an eyewall violation has occurred posterior to
Snellen visual acuity) when compared to use of the limbus and vitreous has presented to the
external magnets is similar; however, the rate wound, the risk of concurrent or delayed retinal
of enucleation is lower in the vitrectomy detachment is high.26–28 Due to this increased
group.6,22,24,25 In practical terms, the use of exter- risk of retinal detachment, there is controversy
nal magnets has all but stopped in the era of about repair strategies for posterior globe lacera-
closed vitrectomy and is primarily of historical tions or ruptures. Specifically, many surgeons
interest. prefer to primarily close the wound only, while
When a metallic IOFB is present, an intrao- others place a prophylactic scleral buckle and/or
cular magnet (rare earth magnet) and/or intra- perform a vitrectomy at the time of primary
ocular forceps can be used to lift the IOFB wound closure.
from the retinal surface once vitreous removal Proponents of prophylactic scleral buckling
is complete.8,12 In addition to new surgical cite studies showing approximately 60–70% of
211
Ocular trauma
posteriorly traumatized eyes will eventually visual axis due a disrupted lens, and in perforat-
require a scleral buckle.26–28 Vitreous disruption ing ocular injuries.5,6,8,18,24,32,33,35–39 In performing
and/or incarceration at the site of primary injury a primary vitrectomy, potential areas of vitreo-
leads to vitreous-eyewall adhesions and overlying retinal adhesion can be eliminated, theoretically
vitreous organization and contraction. An adja- reducing the likelihood of a delayed tractional
cent or distant tractional retinal detachment retinal detachment. 30,40–42 However, performing
can result from the combined forces of the new vitrectomy at the time of primary repair can be
vitreous adhesion to the eyewall, the vitreous difficult. Challenges in primary vitrectomy
contraction, and the contraction of the posterior include induction of a PVD mechanically (par-
hyaloid (in the absence of a PVD).29,30 By placing ticularly in young patients), a limited view of the
a scleral buckle, it is possible to reduce the ante- posterior segment due to poor corneal clarity,
rior–posterior traction that results from vitreous concern for a large choroidal hemorrhage and the
contraction, theoretically reducing the risk of inability to maintain a constant intraocular pres-
tractional retinal detachment. Additionally, an sure if leakage occurs at a penetrating or perfo-
encircling scleral buckle will reduce the effects rating injury site. 36
of centripetal forces at the vitreous base that Alternatively, some practitioners advocate
develop with vitreous contraction and organiza- early vitrectomy, but not at the time of primary
tion of the anterior vitreous. Other reports favor globe repair. In this case, a delayed vitrectomy
prophylactic scleral buckle placement at the time is performed approximately 7–10 days after
of primary repair because ocular muscles are injury.26,27,36 Proponents feel that posterior vitre-
frequently already exposed during surgical ous separation has likely occurred while signifi-
exploration and future placement can be more cant vitreous organization and contraction has
difficult due to subsequent scarring.28 yet to occur. In addition, if subretinal and/or
Scleral buckle placement at the time of open choroidal hemorrhage is present, then delaying
globe repair is not without risks. Since intraocu- vitrectomy permits spontaneous resolution.
lar pressure may be reduced, the extra manipula- Finally, delaying vitrectomy allows time for
tion required to place the scleral buckle increases reduction in uveal congestion, which theoreti-
the chances of a choroidal hemorrhage or extru- cally reduces the incidence of intraoperative
sion of intraocular contents through an occult hemorrhage. 36
posterior eyewall defect. Furthermore, if the Finally, whether to use a scleral buckle and
globe anatomy is significantly altered after repair, pars plana vitrectomy despite the absence of a
anchor scleral suture placement can be more dif- retinal detachment is also controversial. Argu-
ficult to execute, and the risk of a full-thickness ments for using a scleral buckle at the time of
suture pass may increase. In addition to the vitrectomy include:
intraoperative difficulties inherent in placing a 1. The retinal periphery is often difficult to visu-
scleral buckle, the usual postoperative issues alize and peripheral pathology can possibly be
such as induced myopia and diplopia remain. missed.24,43
Vitrectomy alone is sometimes advocated at 2. A scleral buckle gives support to the vitreous
the time of primary open globe repair. 31–34 Most base as the vitreous contracts.24,43
agree that vitrectomy benefits eyes with IOFB, 3. A scleral buckle can prevent traction on the
endophthalmitis secondary to trauma, occluded vitreous base created by incarcerated vitreous
212
in the sclerotomies or at the initial injury retinal detachment, and there are no signs of
site.24,43,44 endophthalmitis.
Most studies suggest that adding a scleral
buckle at the time of vitrectomy can reduce the ENDOPHTHALMITIS
chance of a retinal detachment two to three
times.1,26,27,43,45–47 However, confl icting results Prophylaxis
have done little to ameliorate the controversy.48 In evaluating treatment options for an open
globe injury, the practitioner must determine
INTRAOCULAR LENS IMPLANTATION whether antibiotics are necessary as a preventa-
DURING OPEN GLOBE REPAIR tive measure. Endophthalmitis following an open
globe injury occurs in 2–13% of cases (Figure
Traumatic cataracts are a common occurrence 14.2).14,54 In eyes with retained intraocular
with open globe injuries. If the crystalline lens foreign bodies, the rate of endophthalmitis is
is removed at the time of primary repair, then usually even higher (7–30%), particularly if
the decision to place an intraocular lens (IOL) organic contaminants are introduced into the
at the time of the surgery has to be made. Con- eye.5–17 Currently, in the setting of an open globe,
current IOL placement may allow for more antibiotics are often used despite the lack of
rapid visual rehabilitation. Most published defi nitive evidence to support the practice.
reports have limited investigation to cases in Determining the spectrum of coverage and route
which the trauma involves only the anterior of delivery are thus the main questions that
segment or the eyewall violation is confi ned to arise.
the cornea.49–53 When lacerations or ruptures When choosing an antibiotic, the spectrum of
extend beyond the limbus, the rate of complex coverage is most frequently determined accord-
retinal detachments and proliferative vitreoreti-
nopathy are increased. Subsequent vitreoretinal
intervention can potentially be more compli-
cated with an IOL in place.49
Potential disadvantages to primary IOL implan-
tation include: 49
1. build-up of inflammatory debris on the IOL
2. difficulty in implanting the correct IOL
power
3. the potential need for future posterior segment
surgery
4. endophthalmitis.
Currently, in open globe cases with a concurrent
traumatic cataract, caution and careful case Figure 14.2 This 17-year-old male developed fulminate
endophthalmitis following ruptured globe repair. No
selection are required before IOL implantation.
prophylactic intraocular antibiotics were used at the
The authors recommend limiting primary IOL time of repair. Controversy exists as to whether such
implantation to eyes where the eyewall violation cases could be minimized with the routine use of
is limited to the cornea, there is an absence of prophylactic intraocular antibiotics.
213
Ocular trauma
ing to the method of injury and the organism directly into the vitreous cavity 3–4 millimeters
found most frequently in that type of injury. For posterior to the limbus. Our fi rst line choice of
example, in trauma, the most common organism intravitreal antibiotics in a traumatic setting are
is Staphylococcus epidermis (20.8%). Propionibac- vancomycin (1 mg in 0.1 cc) and ceftazidime
terium acnes (14.6%), other coagulase negative (2.25 mg in 0.1 cc). We prefer to inject antibiot-
Staphylococcus species and Streptococcus viridans ics at the end of the case, after the wound is
group (12.5%) species are also prevalent, though closed. With the availability of a fourth-
infections from the last are found more often in generation fluoroquinolone with known intravit-
children than in adults.54 Aerobic gram positive real penetration and broad-spectrum coverage,
rods (12.5–25%), such as Bacillus species, are the authors also recommend both peri- and post-
also cultured with regularity in open globe inju- operative oral antibiotic coverage. Specifically,
ries, more commonly associated with injuries we prefer to dose gatifloxacin 400 mg daily by
involving soil contamination.54 mouth for 7–10 days after surgery.
Though most practitioners employ subcon-
junctival antibiotics following open globe repair,
there is no consensus about the necessity for Management
intravitreal antibiotics. In cases where there is a Management of post-traumatic (as well as post-
grossly contaminated wound or a high index of operative) endophthalmitis remains contro-
suspicion for organic contamination, the use of versial despite a prospective, randomized,
intravitreal antibiotics is warranted. Vancomycin multicenter study. The Endophthalmitis Vitrec-
and cefazolin have good gram positive coverage. tomy Study (EVS) investigated the issue in the
Ceftazidime has good gram negative coverage. non-traumatic post-cataract surgery setting.
Aminoglycosides are usually contraindicated In the EVS, vitreous tap and injection appeared
intravitreally due to retinal toxicity. Animal as effective as vitrectomy when the visual
models suggest that fluroquinolones can be used acuity is equal to or better than hand motions
and can provide broad-spectrum microbial cov- at presentation. Eyes with light perception
erage. Caution is necessary with any intravitreal vision fared better with vitrectomy.55 Whether
injection if the view of the posterior pole is the results of the EVS can be extrapolated
obscured. Inadvertent injection into the wrong into other clinical scenarios such as trauma is
compartment of the eye can occur due to unrec- unknown.
ognized hemorrhagic or serous choroidal detach- In post-traumatic endophthalmitis, the ratio-
ments. Direct retinal toxicity from the antibiotics nale for vitrectomy over vitreous tap and injec-
is also a concern, particularly if full doses of tion is the mechanical removal of toxins, debris,
intravitreal antibiotics are used in an eye with a and infectious organisms. Removing the vitreous
decreased vitreous volume (e.g. traumatic retinal may also allow better dispersion of antibiotics in
detachment). the vitreous cavity.
In the setting of open globe injury, the authors In cases of traumatic endophthalmitis, the
recommend the use of intraocular antibiotics in authors typically recommend vitrectomy if a safe
certain high-risk clinical settings, such as intra- view of the posterior segment is at all possible,
ocular foreign body, a dirty wound involving as most patients with traumatic endophthalmitis
plant or vegetable matter, or a wound involving will eventually require vitrectomy for visual
the lens. Antibiotics are typically injected rehabilitation.
214
PRIMARY ENUCLEATION AFTER SEVERE be made on an individual basis with careful con-
OCULAR TRAUMA sideration to the individual patient and the status
on the injured globe. In our experience this is an
In cases of severe ocular trauma resulting in unusual occurrence typically reserved for devas-
severe loss of ocular tissue, complete destruction tating injuries with massive loss of tissue (e.g.
of the globe, expulsive choroidal hemorrhage, or gunshot wounds).
severing of the optic nerve, the chances of visual
recovery can be zero. In cases where visual recov- SUMMARY
ery is not possible following severe ocular trauma,
previous studies have recommended enucleation 1. The timing of IOFB removal is dictated by
within 2 weeks due to the risk of sympathetic IOFB composition, risk of infection, and sur-
ophthalmia. Most cases of sympathetic ophthal- gical risks.
mia occur between 2 weeks and 3 months (65– 2. Vitrectomy has revolutionized the removal
80%) post-trauma.56,57 of ferromagnetic posterior segment IOFB,
Loss of light perception is not a contrain- although an improved rate of visual acuity
dication to globe-salvaging surgical repair, as outcomes has never been shown compared to
reversal of loss of light perception has been use of an external magnet.
reported.58 Multiple factors, including anato- 3. IOL implantation at the time of open globe
mical status of the injured eye, mental status of repair is typically reserved for traumatic cata-
the patient, and status of the other eye should racts associated with lacerations or ruptures
be considered in determining the appropriate confi ned to the cornea.
surgical plan. 4. Although controversial, prophylactic scleral
Controversy exists over the use of enucleation buckle following open globe injury may
as a primary procedure. When patients have sus- decrease the rate of subsequent retinal detach-
tained severe and irreparable injuries to the ment, particularly when vitreous incarcera-
globe, they are often sedated with pain medication of the wound is encountered.
tions, unconscious, or even intoxicated. Due to 5. Theoretic advantages of vitrectomy for post-
their altered mental status, they may be tempo- traumatic endophthalmitis include mechani-
rarily incapable of comprehending the severity of cal removal of debris and infectious material
their injuries, and may also be incapable of giving as well as better dispersion of intravitreal
informed consent for globe repair, much less antibiotics.
removal. In such cases, most practitioners advo- 6. Primary enucleation following open globe
cate a primary closure attempt. If the globe injury is seldom performed.
cannot be closed, enucleation can be discussed
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What are some of the major causes of ocular trauma?

What are some of the major causes of ocular trauma?

What are some prevention strategies discussed for reducing ocular injuries?

What are some prevention strategies discussed for reducing ocular injuries?

1

Epidemiology and economic

EPIDEMIOLOGY OF OCULAR TRAUMA

Table 1.1 Physical characteristics of various sporting balls commonly encountered in

Ball type Diameter Max velocity Weight Distensibility

Tennis ball 6.5 cm >150 kph 57 g Moderate

Racquetball 5 cm >150 kph 40 g Signiﬁcant

Hockey puck 2.54 cm vertical >150 kph 160 g None

Paintball pellet 1.72 cm 90–150 mps 3.2 g Signiﬁcant

in 1985 and published in 1988.26 The direct cost,

______________________________________________________________________ REPAIR EXTRAOCULAR MUSCLE: 60.0

INTRODUCTION A number of professional organizations are

organization. More information is available at organization works to educate the public

In industrialized countries, approximately 14%

Figure 2.3 Welding masks that meet or exceed ANSI

splash, irritating mists, vapors, and fumes. OSHA

probability of injury that may require treatment.

Number of blinding injuries

Table 2.2 Recommended eye protectors for selected sports.

Sport Minimal eye protector Comment

eye protectors when involved in high eye risk

has increased in popularity tenfold since 1989.15

Violence is a signiﬁcant cause of ocular trauma. CONCLUSION

Appendix: Eye protection standards and guidelines

American National Standards Institute:

ANSI Z80.1 Requirements for ﬁrst quality prescription ophthalmic lenses

Recreation, hobbies, occupation

American National Standards Institute:

ANSI Z87.1 Practice for occupational eye and face protection

American Society for Testing and Materials:

REFERENCES 10. International Federations of Sports Medicine. Position

GENERAL MEDICAL EVALUATION1,2 other symptoms such as pain, diplopia, and

speciﬁc scenarios in which they add to the diag-

system as well as possible intracranial pathology. Baseline

The pupils may provide the only information

such as epidural or subdural hematomas. A ﬁ xed

to the third cranial nerve, its nucleus, or the

thy) or diffuse retinal injury (e.g. retinal detach-

Hemorrhage-associated Decreased aqueous production Cyclodialysis

Anterior chamber inﬂammation

Closure of cyclodialysis cleft

Increased intraorbital pressure

late canalicular lacerations should be avoided, as Conjunctiva1,3,4

can be aided by the use of staining with ﬂuores- A

Figure 3.5 A 52-year-old male presents with pain and

Descemet’s membrane and the corneal endo- Anterior chamber1,2

iris should also be inspected. An abnormal

posterior segment can be assessed with an

eral and macular), dialysis, and detachment.

Table 3.2 Normal visual acuity in children as measured by various tests

Age (years) Vision test Normal acuity

0–2 Visual evoked potential 20/60–20/20 (6 months)

0–2 Forced choice preferential looking 20/200 (6 months)

0–2 Fixation behavior Central, steady, maintained

0–3 Opticokinetic nystagmus test 20/200 (6 months)

2–5 Allen pictures 20/40–20/20