1
Epidemiology and economic
impact of ocular trauma
James T. Banta
EPIDEMIOLOGY OF OCULAR TRAUMA
Make no mistake, ocular trauma is a disease. It
has a well-established natural history, modifiable
risk factors, and distinct prevention, classifica-
tion, and treatment schemes. The literature is
replete with reports of ocular trauma, both visu-
ally significant and insignificant. Unfortunately,
the vast majority of these studies are hampered
by their retrospective nature and extrapolation to
larger, often very different populations. However,
when the ocular trauma literature is viewed as a
whole, multiple aspects are incredibly consistent:
1. Ocular trauma is a disease with a bimodal age
distribution, the fi rst in the years of late ado-
lescence and early adulthood and the second
in those older than 70.1–3
2. Ocular trauma, particularly severe, vision-
threatening eye injuries, affects men three to
five times as frequently as women.1,3–8
3. Ocular trauma is a significant cause of visual
loss, especially in lower socioeconomic strata
and underdeveloped countries.5,9,10
4. Ocular trauma is largely preventable, espe-
cially in the workplace.6,11–13
5. Ocular trauma is a recurrent disease.4
A large worldwide meta-analysis of eye injury
epidemiology was performed by the World
Health Organization and published in 1998.14
The analysis compiled information from various
studies performed between 1971 and 1995.
Several salient points emerged:
1. 55 million eye injuries which restrict activities
for ≥ 1 day occur annually
2. 750 000 eye injuries require hospitalization
annually
3. 200 000 open globe injuries occur annually
4. 19 million people are unilaterally blind, 2.3
million have bilateral low vision, and 1.6
million are bilaterally blind due to eye
injuries.
The lifetime prevalence of eye injury in three
large epidemiologic studies was approximately
20%.4,15,16 Interestingly, a person with an eye
injury is three times more likely to have a second
eye injury.4 After spending 5 years in an eye
emergency room, I can defi nitively say that
ocular trauma is a recurrent disease. It is remark-
able how often a patient with a metallic corneal
foreign body has multiple corneal scars from pre-
vious foreign body removals. Similarly, assault-
related trauma, particularly fi st-fighting, has a
distinct pattern of recurrence.
Severe eye trauma may slowly be decreasing in
incidence in large part due to improved safety
standards in the workplace. However, it is clear
that current prevention strategies are woefully inad-
equate. Studies have shown that appropriate eye
protection is rarely in place at the time of a
severe eye injury.6,11–13 A study in Singapore
revealed a troubling trend.13 Of a cohort of eye
injuries seen in an emergency department, 71.4%
were work-related. Of these work-related cases,
21.7% wore eye protection, 43.7% were given eye
protection but did not use it, and 34.6% were
not provided eye protection. A study in the
United States of open globe injuries suffered at
work discovered a mere 6% wore eye protection
at the time of injury.11
Cases of eye injuries requiring hospitalization
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
Baseball 7.62 cm
Tennis ball 6.5 cm
Racquetball 5 cm
Hockey puck 2.54 cm vertical
7.62 cm horizontal
Paintball pellet 1.72 cm
cm = centimeter, kph = kilometers per hour, mps = meters per second, g = grams.
of a major decrease in the number of severe eye
injuries, but because of changing indications
for hospitalization.2 Patients with a traumatic
hyphema, now typically observed on an outpa-
tient basis, were routinely hospitalized for 5–7
days in years past. Likewise, the frequency and
duration of hospitalization for open globe inju-
ries has decreased.
Ocular trauma in children has been exten-
sively studied. During the fi rst few years of life,
the incidence of ocular injury is essentially equal
in males and females, but changes quickly to the
male preponderance seen in adults.10 The major-
ity of injuries occur at home or school.17–19 Lower
socioeconomic and educational standing seem to
increase the risk of injury.10 Adult supervision
clearly decreases the incidence of eye injuries in
children.10,18 Scissors and furniture were found
to be frequent causes of severe eye injuries in
children less than 6 years old, while toys, balls,
and stones were more frequently implicated in
children 6 years of age or older.17 Following
ocular injury in children, the rate of blindness
(visual acuity <20/200) ranges from 1% to
34%.10,19–21
Sports activities are a significant cause of ocular
trauma. The protective bony orbit measures
2
Max velocity Weight Distensibility
>150 kph 145 g Minimal
>150 kph 57 g Moderate
>150 kph 40 g Significant
>150 kph 160 g None
90–150 mps 3.2 g Significant
3.5 × 4.0 cm. Use of a ball, projectile, or playing
object (e.g. stick, bat, racket) small enough to fit
within the orbit greatly increases the risk of
severe eye injury (Table 1.1). Eye injuries have
been described in virtually every major and
minor sport. The most common and devastating
offenders are hockey, racket sports, baseball, and
more recently, paintball (often referred to as
‘war games’). In our recent experience, paintball
injuries are rapidly becoming the most common
and severe of the sports-related ocular injuries
encountered (Figure 1.1). The number of patients
and severity of injury encountered with this
activity is rapidly moving into the realm of a
public health crisis. As will be discussed in the
following chapter, certain sports have shown a
dramatic reduction in the number of eye injuries
when the proper eye protection is utilized.
Motor vehicle accidents (MVA) are another
source of eye injury that has been individually
examined. The question has arisen, ‘Do airbags
increase the rate of ocular injury during a motor
vehicle accident?’ Confl icting results are found
in the literature. A large study that reviewed
22 236 MVA with frontal airbag deployment
found an increase in minor eye injuries (specifi-
cally corneal abrasions) and a decrease in severe
 Epidemiology and economic impact of ocular trauma
Figure 1.1 An 11-year-old boy was struck with a
paintball pellet leading to hyphema and extensive iris
disruption.
eye injuries.22 A study out of Henry Ford Hospi-
tal found the rate of MVA-related ocular injuries
was reduced by the use of airbags, as was the
death rate.23 A large meta-analysis published in
2003 found the risk of a severe eye injury due to
airbag deployment to be 0.4%.24 The most recent
epidemiologic study showed a two-fold increase
in eye injuries with airbags and a two-fold
decrease in eye injuries with seatbelt use.25 In
short, it appears that although airbags may
increase the overall rate of eye injuries, the
protective effect against severe eye injuries, and
particularly death, outweighs the small risk.
ECONOMIC IMPACT OF
OCULAR TRAUMA
What is the economic impact of ocular trauma?
Simply put, immense. It is difficult to quantify
precisely because of the significant impact of
indirect costs, particularly lost work days. Only
a few studies looking at the economic impact of
ocular trauma have been published.
An epidemiologic study of eye trauma at an
urban eye emergency department was conducted
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
from California hospitals during a 1-year period,
was $99.7 million for the year 2000.27 As large
as this number is, it only represents a small frac-
tion of the cost when physician fees, laboratory
and radiologic exams, drugs, rehabilitation, and
particularly lost work days are taken into
account.
It is clear that prevention of severe eye injuries
is an accomplishable goal and one that demands
attention given its far-reaching societal and eco-
nomic impact. Ocular trauma is a public health
problem with identifiable prevention strategies.
The following chapter will review these preven-
tion strategies in detail.
FUTURE DIRECTIONS
Compiling epidemiologic data on ocular trauma
is a vital part of defi ning populations, risk factors,
and trends in this disease state. The World
Eye Injury Registry (WEIR) was established to
collect information from ophthalmologists on
severe, vision-threatening eye injuries. Standard-
ized reporting forms are used to capture data at
the initial visit (Figure 1.2) and 6 months after
the initial injury. The standardized nature of the
information gathered allows accurate compari-
sons to be made. Further information is available
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

Prevention of eye injuries
Paul M. Gallogly, Stephanie L. Vanderveldt, James T. Banta
INTRODUCTION
The vast majority of eye injuries are preventable
with currently available protective devices.
Nevertheless, nearly 55 million eye injuries that
restrict activities for more than 1 day occur each
year.1 As eye care professionals we must identify
and educate those individuals at risk for ocular
injury.
The initial step in preventing ocular injury is
identifying patients at risk. One may argue that
the entire population carries some inherent risk.
This of course is true, but identification of
patients with high-risk jobs or activities may
help limit preventable ocular trauma. A simple
history of daily activities and hobbies obtained
by the ophthalmologist or technician can quickly
and easily identify these patients. Brief questions
may include: ‘What are your hobbies?’ ‘Are you
involved in sports activities?’ ‘What is your
occupation?’ A previous history of ocular trauma
is equally important, as studies have shown that
ocular trauma is a recurrent disease.2
Another important population that must be
identified is the patient with one functional eye.
The functionally one-eyed patient is an individ-
ual who would have a significant change in life-
style if the better-seeing eye was damaged or
lost. Some common examples include patients
with amblyopia, decreased vision due to a prior
traumatic event, or decreased vision due to a
chronic but asymmetric ocular condition (e.g.
glaucoma). After the ophthalmologist has appro-
priately identified those individuals with preven-
tative needs, recommendations must be given in
a simple and directed manner.
2
A number of professional organizations are
involved in the standards of eye protection
manufacturing, testing of eyewear to conform
to safety standards, and dissemination of safety
information to educate the public. They
include:
1. ANSI: The American National Standards
Institute is an organization which facilitates
voluntary consensus standards in the US and
abroad. ANSI is a private, nonprofit organiza-
tion that promotes voluntary consensus stan-
dards including standards for eye protection,
both personal and occupational. ANSI pro-
vides standards for the strength of polycar-
bonate lenses and the manufacture and design
of safety spectacle frames and chemical
eyewash stations, among many other safety
standards. More information is available at
www.ANSI.org.
2. ASTM: ASTM International, formerly the
American Society for Testing and Materials,
is a voluntary standards development organi-
zation generating standards for the manufac-
turing of a wide variety of materials including
sports eye protectors. ASTM International
certifies racket sport eye protectors as well as
those for paintball, baseball, downhill skiing,
and ice hockey. The ASTM standards for
racket sport wear are significantly more strin-
gent than those of ANSI. More information is
available at www.ASTM.org.
3. PECC: The Protective Eyewear Certification
Council independently tests and certifies
eyewear in hopes of reducing eye injuries.
Manufacturers that produce products passing
their standards bear the seal of the
7
 Ocular trauma
organization. More information is available at
www.PROTECTEYES.com.
4. CSA: The Canadian Standards Association
works to develop standards for a multitude of
items, particularly items meant to enhance
public safety. They also work to educate the
public about these standards. More informa-
tion is available at www.CSA.ca.
5. HECC: The Hockey Equipment Certification
Council independently reviews the recom-
mendations of various hockey organizations
with regard to safety equipment and certifies
specific safety products by validating the
testing performed by the manufacturer. This
organization is supported by USA Hockey
who require the use of HECC-certified equip-
ment in official play. HECC refers to ASTM
F513 guidelines in certification testing of all
eye and face protectors. More information is
available at www.HECC.net.
6. NOCSAE: The National Operating Commit-
tee on Standards for Athletic Equipment is
involved in testing and implementing test
standards for various sports in a concerted
effort to reduce injuries. More information is
available at www.NOCSAE.org.
7. OSHA: The Occupational Safety and Health
Administration is a component of the US
Department of Labor that establishes stan-
dards to ensure the safety and well-being of
American workers. In particular, OSHA
governs the requirements for use and mainte-
nance of occupational eye protection in various
industrial settings. The organization also pro-
vides employee training requirements for the
use of protective equipment and the care,
maintenance, and inspection of such equip-
ment. More information is available at www.
OSHA.gov.
8. AAO: The American Academy of Ophth-
almology is the professional society of
ophthalmologists in the United States. The
8
organization works to educate the public
about ocular public health issues, including
prevention of ocular injuries. More informa-
tion is available at www.AAO.org.
Given the sheer number of high-risk activities,
the scope of this chapter does not allow the
authors to cover each activity in detail. Special
mention will be given to a few high-risk situa-
tions that are most frequently associated with
eye injuries, namely: work, sport, driving, and
assault.
LENS MATERIALS
Glass or allyl resin plastic (CR-39) lenses, present
in nearly 90% of all dispensed spectacles, have
little impact resistance, are prone to shatter, and
have caused eye injury as a result of this shatter-
ing. The material of choice for all protective
lenses, both street-wear and active-wear, is poly-
carbonate. Polycarbonate lenses have excellent
impact resistance, good optical properties, and
acceptable UV absorption. They are thinner,
lighter, equally scratch resistant, and significantly
safer than glass or CR-39 plastic lenses.
Polycarbonate lenses are not without limita-
tions, however. First, there is a cost differential
of approximately $25 for polycarbonate lenses
vs. CR-39. Additionally, there is a limitation in
the range of refractive errors that can be accom-
modated. Most companies can accommodate
refractive errors of 12–14 diopters of myopia.
Recently, with refi nements of high-index poly-
carbonate, prescriptions can be fi lled up to 20
diopters of myopia, albeit at a premium cost.
Chromatic aberration at the lens periphery of
high minus polycarbonate lenses is also encoun-
tered. Athletes or workers with a large refractive
error that precludes the use of polycarbonate
should wear contact lenses with the appro-
priate non-prescription polycarbonate protective
device.
 Prevention of eye injuries

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

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
 Prevention of eye injuries

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
Figure 2.5 Polycarbonate sports goggles that meet or
exceed ASTM F803 should be used for all high-risk
sporting activities, particularly racket sports. Many
models can have prescription lenses fitted. (Photo
courtesy of Hilco.)
2. Sports frames with 3 mm polycarbonate lenses.
Frames which meet ASTM standard F803 cri-
teria are required for use by persons engaged
in high eye risk activities and non-collision
sports (racket sports, baseball fielders, basket-
ball, soccer) and for all functionally one-eyed
patients engaged in any sporting activity
(Figure 2.5).12 Although ASTM criteria are
specifically applied to eye protectors for racket
sports, it is generally recommended that these
be used for other non-collision sports as
well. There are presently no standards for
non-collision sports such as soccer and basket-
ball. Sports participants without refractive
error or who wear contact lenses should
wear non-prescription polycarbonate sports
14
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
baseball/softball batter and catcher face
shields, football helmets, lacrosse helmets
with faceguards, polo helmet-mounted eye
protection, and hockey face protectors and
helmets through the National Operating
Committee on Standards for Athletic Equip-
ment (www.NOCSAE.org).
Functionally one-eyed patients should be dis-
couraged from participating in very high eye risk
sports such as boxing, full-contact martial arts,
and wrestling. These activities not only pose
extreme danger to the eyes, but also do not allow
for the reduction of risk by the use of protective
devices.
Paintball
Paintball is a relatively new sport in which par-
ticipants play various war games using guns to
shoot opponents with small paint-fi lled projec-
tiles. The compressed air or gas rifles used in the
sport have a muzzle velocity of 80–130 m/sec.14
In the United States, participation in paintball

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
United States rose from an estimated 545 in
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
could have been prevented by the use of proper
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-
tection immediately prior to injury.13 Profes-
sional paintball tournaments and commercial
venues have stringent, enforced safety require-
ments. In these settings, paintball can be a rela-
tively safe activity. However, players sometimes
remove their protection because they are not
involved in the active game or they feel the pro-
tection is too warm to wear. There is also a trend
away from commercial vendors and towards non-
commercial and private use of paintball devices.
Such a trend may suggest an increase in the use
of paintball weapons in unsupervised locations
without proper protective devices. Parents need
to be informed of the inherent dangers of paint-
ball equipment and should keep it locked away
as they would any fi rearm, allowing it to be used
only in organized and supervised settings.
Although ASTM does not specifically test
paintball goggles, it did release a voluntary
standard for paintball goggle testing (ASTM
F1776-01). When advising a patient, make
certain that goggles developed specifically for
Prevention of eye injuries
Figure 2.6 Eye protection for paintball-related
activities should meet or exceed ASTM F1776. (Photo
courtesy of Draxxus/VForce Paintball.)
paintball that meet or exceed ASTM F1776 are
utilized (Figure 2.6).
AIRBAG INJURIES
In the United States the use of both driver and
passenger side airbags in conjunction with three-
point lap restraints was mandated in 1997.
Deployment of an airbag occurs in three steps.
In the fi rst step sensors detect a crash. This
results in rapid oxidation of a propellant that
inflates the bag at a velocity of 100–200 mph.
Talc is used in the packaging of the airbag and is
also released in the process. Gases are vented to
partially deflate the airbag, softening the occu-
pant’s ‘landing.’ According to statistics on frontal
crashes from the US Department of Transporta-
tion, airbags are estimated to reduce the number
of fatal injuries by 31–32% above and beyond the
45% reduction afforded by seatbelts.18
Although airbags can significantly reduce mor-
tality, they also are associated with serious eye
injury. There is a broad spectrum of eye injuries
associated with airbags including, but not limited
to, burns, lacerations, corneal abrasions, hyphe-
mas, retinal detachments, and ruptured globes.
15
 Ocular trauma
Long-term visual outcome data is not available
because the literature consists largely of case
reports and small case series. The authors are of
the opinion that the life-preserving function of
airbags far outweighs the risk of eye injury.
Research and development by car companies and
engineers aimed at increasing the safety profi le
of airbags while maintaining their life-preserving
function is ongoing. Newer, ‘depowered’ airbags
are now standard on all cars produced after 1997
and have recently been reported to lessen the
risk of eye injury.19
ASSAULT-RELATED INJURIES
Violence is a significant cause of ocular trauma.
In 1992, assault accounted for more than 20% of
the penetrating eye injuries reported to the
National Eye Trauma System Registry. A review
of the literature suggests that assault-related
injuries involve primarily young males, together
with alcohol or drugs, unsettled social environ-
ments, and unemployment. As reported by
Dannenberg et al, a wide variety of objects are
used as weapons in assaults. The most common
object used was the fi st. The protective value of
spectacles could not be assessed in this report
16
because information on the use of eyeglasses was
not provided at the time of data collection.20
The only realistic strategy to reduce assault-
related eye injuries is violence prevention. If
abuse or violence is suspected, directed ques-
tions regarding abusive or violent situations
should be posed. When appropriate, law enforce-
ment and social services should be utilized in
hopes of preventing further violence. Legal
requirements vary, but most states have manda-
tory reporting requirements when abuse is sus-
pected, particularly when children and the
elderly are involved.
CONCLUSION
Prevention of eye injuries receives little of the
attention it deserves. Modifying risk factors and
implementing appropriate eyewear protection
strategies can reduce the rates of ocular injury
while allowing patients to maintain a productive
career and enjoy their leisure time to the fullest.
It is the duty of the eye care professional to be
familiar with the many safety devices and ask
directed questions to help best protect the
patient.
 Prevention of eye injuries

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

History and examination of
the injured eye
Alexei L. Moraczewski
GENERAL MEDICAL EVALUATION1,2
In many cases involving ocular trauma, the oph-
thalmologist is the fi rst physician to assess the
patient. Many patients with ocular trauma also
sustain non-ocular trauma as well; thus it is
crucial to ensure that life-threatening injuries
are not present before focusing attention on the
eye. The initial assessment of the traumatized
patient should include measuring vital signs and
mental status as well as a rapid general physical
examination to exclude any soft tissue or bony
injuries. If conditions such as respiratory dis-
tress, cardiovascular instability, massive bleed-
ing, or an acutely impaired mental status are
encountered, the patient should be transferred
immediately to an emergency room or trauma
center.
Once the general medical stability of the
patient is ensured, a general medical history
should be obtained to document all current and
past medical conditions, previous surgeries,
current medications, known drug allergies, use
of alcohol and illicit drugs, and tetanus immuni-
zation status.
HISTORY1,3
A focused yet careful history is important, as it
often plays a large role in guiding further evalu-
ation and management. The history should be
well documented in the medical record, espe-
cially given the increased incidence of litigation
following ocular trauma. The patient should be
questioned about any sudden or gradual changes
in vision since the time of the trauma, as well as
3
other symptoms such as pain, diplopia, and
photophobia.
The details of the traumatic incident should be
recorded:
1. Date, time and location of the incident
2. Mechanism of injury (struck by fi st, hammer-
ing metal on metal, etc.)
3. Accidental, intentional, or self-infl icted
injury
4. Accident setting (work, home, sports-related,
etc.)
5. Use of contact lenses, corrective glasses, or
safety glasses at the time of accident
6. Presence of witnesses to the accident.
The mechanism of injury is particularly useful
for determining the level of suspicion for intra-
ocular or intraorbital foreign bodies.
In cases of mechanical trauma to the eye with
a foreign object, it is important to note:
1. The physical characteristics of the object
causing the trauma (e.g. size, presence of
sharp edges)
2. The distance and direction traveled to the
eye
3. The location of the impact
4. The condition of any eyewear used at the time
of injury.
An initially high level of suspicion for intraocular
or intraorbital foreign bodies should be main-
tained with any ocular trauma. In highly sus-
pected or confi rmed cases of foreign bodies, the
following information should be gathered:
1. The composition of the foreign body (which
determines its ocular toxicity)
2. The origin of the foreign body (fragment from
a metal tool, glass from a windshield)
19
 Ocular trauma
3. Activity at the time of the injury
4. The possibility of single or multiple foreign
bodies
5. The distance, direction, and speed traveled by
the foreign body
6. The position of the patient’s head and direc-
tion of gaze at impact
7. A description and the composition of tools,
machinery, grinding surfaces, or weapon used
at the time of the injury
8. Possible contamination of foreign bodies
with oil, grease, dirt, or vegetable matter
(to determine the risk of microbiologic
contamination).
Chemical injuries, especially with alkali sub-
stances, are true ophthalmic emergencies, and
immediate irrigation should be initiated prior to
obtaining a detailed history. Once initial treat-
ment has been administered, the following
should be performed:
1. The chemical (acid or alkali) and physical
(liquid, gel, particulate) properties of the sub-
stance should be established.
2. The pH of the substance should be measured
if a sample is available.
If the identity or characteristics of the substance
are unusual or unknown, the local poison control
center can be extremely helpful in providing this
information.
In the uncommon cases of thermal burns,
the type and temperature of the involved mate-
rial and duration of contact should be elicited.
If the trauma involves electrical burns, the
amount of electrical energy involved and the
entrance and exit points should be determined
if possible.
Following injuries from animals:
1. The type of animal and how the injury was
infl icted (e.g. bite, scratch) should be
identified.
2. It should be determined if the attack was
spontaneous or provoked.
20
3. The animal should be located to allow testing
for the presence of transmissible disease, if
necessary.
A brief, directed past ocular history should
include pre-existing ocular conditions, prior
ocular surgeries, and level of vision prior to the
trauma. Previous ocular surgery can increase sus-
ceptibility to traumatic injury. The presence of
intraocular (e.g. intraocular lens) or periocular
appliances (e.g. scleral buckle, glaucoma drain-
age implant) should be noted. Any previous
treatment for the injury should be recorded, in-
cluding self-administered treatment. The routes,
dosages, and timing of any administered medica-
tions should be recorded. The names, locations,
and phone numbers of any physicians who previ-
ously treated the patient should be recorded in
the event that they need to be contacted about
the case.
EXAMINATION
General considerations
The examination of an injured eye is fraught
with difficulty. The anxiety and pain of the
patient with a potentially vision-threatening
injury often makes for a less than desirable
cooperative effort. It is vital to establish a rapport
with the patient and family and quickly lay the
foundation for effective communication and
trust. Simply acknowledging the obvious anxiety
and potential concern of the patient can do much
to alleviate anxiety and allow proper examina-
tion. Furthermore, during the examination,
explaining each step can help calm the patient.
In the setting of a potential open globe injury,
everything must be done to expedite the history
and examination process while minimizing
manipulation of the eye. We routinely put a
metal shield over injured eyes before taking any
history to prevent the patient from touching or

Figure 3.1 Desmarres retractors are used to gently
open the eyelids of a patient with orbital compartment
syndrome.
rubbing the eye. Examination should be carried
out only by those specifically trained to care for
ocular emergencies.
Extensive periorbital swelling and hemorrhage
are often encountered in the acute setting. If the
patient is unable to open the injured eye, the use
of Desmarres eyelid retractors is sometimes nec-
essary (Figure 3.1). These retractors are designed
to minimize anterior–posterior pressure on the
eye while allowing access to the injured eye.
Included
on DVD
Depending on the extent of periocular swelling,
the examiner can sometimes hold a single retrac-
tor under the upper lid and proceed with the
examination one-handed. However, it is some-
times more convenient to have a second trained
staff member hold the eyelid retractors so the
physician is free to use both hands.
Finally, common sense must be emphasized.
Certain examination steps are sometimes de-
ferred in the acute setting. Intraocular pressure
is not checked until the structural integrity of
the eye is confi rmed. Scleral depression, color
vision testing, and forced ductions are not neces-
sary on every patient and should be reserved for
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
function following trauma.
Ideally, the visual acuity should be measured
in each eye separately using a standard Snellen
visual acuity chart. The patient’s corrective
glasses should be used if available. If the patient’s
glasses are not available or the patient’s refractive
error is unknown, pinhole acuity should be mea-
sured. If a standardized distance vision chart is
not available, a near vision card or representative
newsprint can be substituted. Correction of
presbyopia may be required depending on the
age and refractive status of the patient. The
method used to check visual acuity should be
documented in the medical record.
When the vision is too poor to be measured
with a vision chart, a gross assessment of vision
is documented (counting fi ngers at a specified
distance, hand motions, light perception with
or without projection, no light perception). If
the patient is found to have no light perception,
this should be confi rmed and recorded by the
physician using the brightest light source
available (usually an indirect ophthalmoscope)
while occluding the uninvolved eye completely.
Pupils1,3,4
Examination of the pupils provides valuable
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
(e.g. cataract, hyphema, vitreous hemorrhage)
cause an RAPD. An RAPD is detected utilizing
the swinging flashlight test, where a light source
is rhythmically shifted back and forth from one
pupil to the other. An RAPD is present in a pupil
that paradoxically dilates when the light is shone
into it. The swinging flashlight test can be used
even if one pupil is obscured, severely damaged,
or pharmacologically dilated. Using a separate
light source to illuminate the uninvolved pupil,
the test is performed normally, but only the
response of the uninjured or undilated pupil is
monitored. If an RAPD is present in the injured
eye, the reactive uninjured eye will consensually
dilate when the light is directed toward the
injured eye (Figure 3.2). This is sometimes
referred to as an ‘RAPD by reverse.’
22
Dilation
Bright illumination
Figure 3.2 Testing for a relative afferent pupillary defect
when one pupil is obscured or dilated requires
continuous, mild illumination of the normal uninvolved
pupil. We often use the light from a direct
ophthalmoscope turned down to a setting where the
uninvolved pupil is just visible. A second bright light
source is used to test each pupil individually. We typically
use an indirect ophthalmoscope turned up to its
maximum intensity for this purpose. The light source is
swung rhythmically between the two pupils and the
response of the uninvolved pupil is noted. In the absence
of an RAPD, the uninvolved pupil should constrict when
the bright light source is introduced to either eye. An
‘RAPD by reverse’ is present when the uninvolved pupil
paradoxically dilates when the light source is introduced
to the involved pupil, denoting injury to the anterior
visual pathway (typically the optic nerve).

The shape of the pupil should be noted. An
eccentric or peaked pupil may indicate a trau-
matic iridodialysis, iris sphincter tear, vitreous
prolapse into the anterior chamber or an open
globe injury with iris prolapse.
Brightness testing and color vision2,4
Brightness testing is a quick subjective test of
optic nerve function. A bright light source is
shone in the uninjured eye, and the perceived
brightness is assigned a value of 100% or $1.00.
When the light is shone in the involved eye, the
patient should provide the relative amount of
brightness that is perceived (e.g. 50% or 50
cents).
Color vision testing and red desaturation testing
can help assess optic nerve function. Color vision
can be tested using commercially available pseu-
doisochromatic plates (e.g. Ishihara or Hardy-
Rand-Rittler). If color plates are not available, red
desaturation testing can be used. The patient
should look at a red object, typically the cap of a
dilating drop bottle, with each eye separately; if
optic nerve dysfunction is present, the red color
may appear gray or washed out compared to that
seen by the uninvolved eye.
It is important to note that subjective tests
such as brightness and red desaturation testing,
variations in patient understanding and concom-
itant ocular injuries can make interpretation of
the examination unreliable.
Visual fields1,4
In the emergency setting, testing visual fields
by confrontation is effective and efficient. Each
eye is tested separately. With one eye fully
occluded, the patient should fi xate on the exam-
iner’s face. The examiner’s fi ngers are presented
in the four peripheral quadrants and centrally. If
fi ngers from both hands are presented simultane-
ously in different quadrants, visual neglect may
be revealed. A red object may be used if visual
History and examination of the injured eye
acuity is poor or optic nerve dysfunction is
suspected.
Formal visual field testing (e.g. static auto-
mated perimetry or Goldmann perimetry)
usually can be deferred in the emergency setting
unless it is needed for diagnostic purposes.
This requires that the patient is stable, coopera-
tive, and can sit upright. Formal visual field
testing can be a useful method of following
the course of traumatic conditions such as
traumatic optic neuropathy. Amsler grid testing
can be used to detect and follow central
scotomata.
Extraocular motility1,3,4
Extraocular motility testing is especially impor-
tant in cases of known or suspected orbital or
cranial nerve injury. Testing should be performed
after the possibility of an open globe injury has
been excluded in order to minimize ocular
manipulation. Abnormal ductions and versions
should be documented to allow comparison for
future examinations. In some circumstances
(e.g. orbital fracture, traumatic 4th cranial nerve
palsy), diplopia or limitation of movement of the
globe should be measured in prism diopters in
all directions of gaze, and the examiner should
attempt to isolate the affected extraocular
muscle(s) or cranial nerves. This requires ade-
quate vision in both eyes as well as a conscious
and cooperative patient.
If limitation of ocular motility is present,
forced duction testing may allow differentiation
between a paretic and restrictive etiology. Forced
duction testing is performed as follows:
1. Topical anesthetic (e.g. proparacaine) is
administered.
2. A cotton-tipped applicator is soaked in 4%
lidocaine and placed for at least 1 minute on
the conjunctiva over the extraocular muscle
to be tested.
23
 Ocular trauma
3. The muscle insertion is grasped with toothed
forceps, and the eye is rotated in the direction
opposite the muscle being tested.
Resistance to passive motion indicates a restric-
tive etiology. Forced duction testing is typically
reserved for patients with an orbital fracture and
suspected extraocular muscle entrapment.
Intraocular pressure1,3
It is prudent to defer measurement of intraocular
pressure (IOP) until the presence or absence of
an open globe injury is determined. If a known
open globe injury is present, measurement of
IOP in the injured eye should be deferred until
after repair.
Various methods of measuring IOP are avail-
able, including Goldmann applanation tonome-
try, various hand-held tonometry devices
(e.g. Tonopen), pneumotonometry, and Schiøtz
tonometry. Applanation tonometry is the pre-
ferred method, but hand-held devices are
extremely useful if the patient cannot be exam-
ined at the slit lamp. If no devices are available,
globe palpation can provide an extremely gross
estimate of comparative IOP.
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.
External examination1,2
The head, face, periorbital areas, and eyelids
should be examined under good lighting. These
24
areas should be inspected for the presence of
ecchymoses, edema, ptosis, lacerations, and
foreign bodies. The presence of enophthalmos or
exophthalmos should also be noted and may
require the use of a Hertel exophthalmometer.
If ptosis is present, levator function and palpe-
bral fi ssure size should be measured and
documented.
In the case of facial and eyelid lacerations,
dried blood may obscure the underlying tissues
and should be gently cleaned with gauze and
sterile saline or hydrogen peroxide. The edges of
the laceration should be gently separated and the
wound should be fully explored to assess its
depth and the presence of foreign bodies. Wounds
that initially appear relatively superficial often
are found to extend much deeper when they are
properly cleaned and explored (Figure 3.3). In
cases of more severe periorbital injuries it may
be necessary to examine the patient under seda-
tion or general anesthesia in order to assess ade-
quately the full extent of injury.
Attention should be paid to lacerations that
involve the lid margin or the lacrimal drainage
system. The use of toothed forceps to manipu-
Figure 3.3 Eyelid lacerations must be fully explored to
their fullest extent once globe integrity is confirmed
and concomitant ocular injuries have been treated and
stabilized.
 History and examination of the injured eye

Table 3.1 Causes of intraocular pressure (IOP) change following ocular trauma

Causes of high IOP
Lens-associated
• Angle closure glaucoma
secondary to pupillary block from
subluxated or dislocated lens
• Phacomorphic glaucoma
• Lens particle glaucoma
• Phacoantigenic uveitis
Causes of low IOP
Excessive filtration
• Wound leak (e.g. open globe
injury)
• Ciliochoroidal detachment
• Cyclodialysis cleft
• Retinal detachment
Causes of high or low IOP
Traumatic iridocyclitis
• High IOP from inflammatory
cells in anterior chamber
• Low IOP from ciliary body
shutdown

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

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

27
 Ocular trauma
Figure 3.6 A thin slit beam best demonstrates the
depth of the anterior chamber. A contusive injury to
the eye caused a rupture of the anterior lens capsule
and the rapidly progressive cataract seen in this photo.
The anterior chamber depth was severely shallow in
comparison to the fellow uninjured eye.
Gonioscopy allows examination for iridodialysis,
cyclodialysis, angle recession, and foreign bodies
in the angle. This is particularly important if a
small full-thickness corneal wound is present
without further injury to the iris or lens, as
foreign bodies in the inferior angle can easily be
missed without gonioscopy.
The anterior chamber should also be examined
for the presence of cells and flare, indicating a
traumatic iritis. The inflammatory reaction
should be graded to allow comparison with
future examinations. The presence of hyphema
and hypopyon should be noted, and the height
of each in millimeters should be documented.
The presence of fibrin, vitreous, or foreign
bodies in the anterior chamber should also be
noted.
Iris1
The iris should be inspected prior to the instil-
lation of mydriatics, as dilation may obscure per-
tinent fi ndings. The surface of the iris should be
examined for foreign bodies. The contour of the
28
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.
The shape of the pupil should be noted. An
eccentric or peaked pupil may indicate a trau-
matic iridodialysis, iris sphincter tear, vitreous
prolapse into the anterior chamber, or an open
globe injury with iris prolapse.
Lens1,3
The crystalline lens should be examined for its
position, stability, clarity, and capsular integrity.
The presence of lens subluxation or dislocation
should be noted. Phacodonesis, or shaking of the
lens with eye movements, should be specifically
tested. The presence of vitreous around the lens
indicates zonular rupture and lens instability. In
cases of severe trauma, the lens can be extruded
completely from the eye through a scleral or
corneal wound. In pseudophakic patients,
extrusion of an intraocular lens can occur
through dehiscence of a prior surgical wound,
particularly ruptured penetrating keratoplasty
or extracapsular cataract surgery wounds.
The clarity of the lens can be evaluated
with direct illumination and retroillumination.
Numerous lens changes can occur after trauma,
including rosette-shaped posterior subcapsular
cataracts, anterior subcapsular opacities, and
sectoral cataracts. A contusive injury can create
a Vossius ring, a brown ring of pigment on the
anterior lens capsule resulting from forceful
iridolenticular contact (Figure 3.7).

Figure 3.7 A Vossius ring is seen on the anterior lens
capsule following an assault-related contusive injury in
a 42-year-old male. Significant subconjunctival
hemorrhage and a small hyphema are also noted.
It is important to note the integrity of the lens
capsule, as a violation of the capsule may indi-
cate the presence of a foreign body. It is also
important to note any leakage of cortical mate-
rial due to its antigenic nature. Intralenticular
foreign bodies should be noted as well.
General principles of the posterior
segment examination1,2,4
The posterior segment should be examined as
expeditiously as possible since progressively
difficult visualization can occur from corneal
edema, hyphema, traumatic cataract, vitreous
hemorrhage, etc. The type, strength, and time of
mydriatic use should be documented in the
medical record so that subsequent examiners
will not misinterpret the cause of dilated pupils
(on multiple occasions, we have seen CT scans
ordered on post-trauma patients because of
undocumented dilation of the pupils). When an
open globe injury is suspected, any topical medi-
cations should be given from unopened sterile
bottles to avoid possible infection. Pharmaco-
logic mydriasis should be deferred in the case of
an open globe injury with iris prolapse; the
History and examination of the injured eye
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
record.
Vitreous1,4
The anterior, mid, and posterior vitreous should
be examined for the presence of pigment
(‘tobacco dust’), hemorrhage, debris, and foreign
bodies. The presence of a Weiss ring, indicating
a posterior vitreous detachment (PVD), should
be noted. Tobacco dust and/or vitreous hemor-
rhage should prompt a search for a traumatic
PVD or retinal tear. Vitreous streaming toward
the anterior segment or pars plana may reveal an
occult open globe injury. The presence of white
blood cells or purulence in the vitreous cavity
should prompt collection of vitreous samples for
microbiologic identification.
Vitreous in the anterior chamber has a unique
appearance of a gelatinous material with small,
brown pigmented spots intermixed and indicates
significant damage to the zonular apparatus.
Because of the higher molecular weight of vitre-
ous compared to aqueous, the pupil is normally
distorted in the vicinity of vitreous prolapse.
Phacodonesis, lens subluxation, or frank lens dis-
location often coexists with vitreous prolapse.
Retina and choroid1,4
The retina should be carefully and thoroughly
examined for the presence of whitening and
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-
geneous and is a clue to the presence of choroidal
rupture. The area surrounding intraretinal or
subretinal hemorrhages should be carefully
examined for the presence of foreign bodies or
occult open globe injuries.
The choroid should be examined for the pres-
ence of choroidal rupture and choroidal detach-
ment. Choroidal ruptures are often multiple,
concentric to the optic disc, and accompanied by
subretinal hemorrhage.
Optic nerve1
The optic nerve head should be inspected for
the presence of edema and hemorrhage. The size
and shape of the cup should be documented. An
enlarged cup or other signs of previous glauco-
matous damage may require more aggressive
intraocular pressure control as compared to a
normal nerve.
In cases of severe trauma, the optic nerve can
be partially or completely avulsed. This is seen
as an absence of the optic disc or a hole in the
sclera at the site of the disc (Figure 3.8). Despite
significant contusive injury, the optic nerve often
appears normal immediately following trauma
and is therefore of limited value in cases of sus-
pected traumatic optic neuropathy.
Figure 3.8 Peripapillary intraretinal hemorrhage with
breakthrough vitreous hemorrhage following optic
nerve avulsion in a 10-year-old child.
SPECIAL CONSIDERATIONS FOR
PEDIATRIC PATIENTS5
The history in cases of pediatric ocular trauma
is frequently elicited from the child’s caregiver
(usually the child’s parents). However, in cases
of poor supervision or child abuse, the history
from the caregiver may not be accurate. Older
children sometimes fear disciplinary action and
may not provide the entire truth if they were
engaged in prohibited activities.
Examining the eyes of a child is challenging
under ideal circumstances and can verge on
impossible when a child is injured. Establishing
a rapport and interacting with the child in a
game-like fashion may help maintain the child’s
attention. The noncontact portions of the exam
should be performed fi rst, and no pressure should
be placed on the globe. Explaining each part of
the exam as it is performed may reduce anxiety
on the part of the caregiver.
For children between the ages of 10 weeks and
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
 History and examination of the injured eye

be a colorful toy or an adult’s face, but should
not be a light source. It should be confi rmed that
the child is following the visual stimulus and not
any auditory stimuli that may arise from it. For
older children, visual acuity can be assessed with
Allen cards, HOTV letters, the tumbling E
game, or standard visual acuity charts depend-
ing on the child’s age and education level
(Table 3.2).
If an infant or toddler is very uncooperative,
the child can be restrained in a commercially
available or makeshift papoose. A pediatric
eyelid speculum with the use of topical anesthe-
sia can be used, but only if an open globe injury
is not suspected. Toddlers can also be restrained
as follows:
1. An assistant and caregiver sit facing each other
at the same level.
2. The child is placed supine with legs straddling
the caregiver’s waist.
3. The child’s head is placed on the assistant’s
lap.
4. The caregiver holds the child’s hands and the
assistant holds the child’s head still while the
physician examines the child.
Sometimes it is more feasible for the physician
to take the place of the assistant and control the
head with his legs while performing the exami-
nation (Figure 3.9).
If the above methods are not sufficient or if an
open globe injury is suspected, the child should
be examined under conscious sedation or general
anesthesia. This should be carried out under
the supervision of a qualified anesthesiologist.
Vital signs should be monitored during the
examination, and advanced cardiopulmonary
life support measures must be present and
available. Pediatric clearance should be obtained
prior to any examination requiring general
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 3.9 Examination technique for pediatric
patients. The parent or guardian controls the legs
and arms while the physician controls the head.
Alternatively, an assistant can be seated opposite the
parent and control the head leaving the physician with
more flexibility to examine the patient.
Examination of the anterior segment can be
facilitated by a penlight or portable slit lamp. If
the child is old enough to undergo a conventional
slit lamp examination, he or she can sit on the
caregiver’s lap, kneel on the exam chair, or stand
on the exam chair’s step. Alternatively, an indi-
rect ophthalmoscopy lens with a light source
(e.g. indirect ophthalmoscope) may provide
enough magnification to examine the anterior
segment. All light sources should be used at low
intensity if possible.
Eye drops are often a source of anxiety for
children. For mydriasis, a combination of
phenylephrine 2.5%, tropicamide 0.5%, and
cyclopentolate 0.5% can be prepared so that
all three medications can be instilled with
one drop. Instilling topical anesthesia prior to
mydriatics can reduce discomfort and increase
cooperation.
Child abuse
The ophthalmologist should be alert for ocular
and systemic signs of child abuse. Child abuse
32
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
proceedings are commonplace. The assailant in this
case was a family member acting as a babysitter for the
infant.
should be suspected when the caregiver’s history
is inconsistent, the child has a history of multiple
emergency room visits, or the character of the
injury is not compatible with the caregiver’s
history. The ocular examination can play an
important role in the diagnosis of shaken baby
syndrome. In this syndrome, intraocular and
intracranial hemorrhages are present, often
without external signs of trauma. Ocular hemor-
rhages are usually intraretinal but can be prereti-
nal or subretinal as well (Figure 3.10).5
Physicians are legally mandated to report
cases of suspected child abuse to the appropriate
social service agency or the police. A reason-
able suspicion of child abuse exists when it is
part of the differential diagnosis. Most states
have laws protecting a reporting practitioner
with good intentions from civil liability. Failure
to report is a misdemeanor in most states.
Accurate and detailed documentation of the
history and examination in the medical record
(including photography if available) is of
utmost importance, as this information often
is submitted as evidence in a deposition or trial.
The examining physician should also expect

to serve as a material witness for any legal
proceedings.6
SPECIAL CONSIDERATIONS FOR
ELDERLY PATIENTS4
As with pediatric patients, some elderly patients
may not be able to provide an adequate history
because of underlying disability or dementia.
The history is often elicited from family members
or caregivers, but the history may not be accurate
if elder abuse is involved.
Falls are a common cause of injury in elderly
patients, and it is important to investigate the
circumstances surrounding the fall. Many falls in
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-
diovascular dysfunction (e.g. arrhythmia, hypo-
tension) that warrants further attention.
Ocular and periocular injuries from falls in the
elderly are frequently associated with systemic
injuries, often serious. These include fractures
(hip, long bones, skull, wrist) and internal
hemorrhage (intracranial, intra-abdominal). The
latter may be facilitated by anticoagulation
therapy. If the ophthalmologist is the fi rst physi-
cian to encounter such a patient, a rapid assess-
ment for these injuries should be performed
before focusing attention on the eye. Conditions
such as respiratory distress, cardiovascular
instability, massive bleeding, or acutely impaired
mental status require immediate transfer to an
emergency room or trauma center.
As with child abuse, a high level of suspicion
should be maintained about the possibility of
elder abuse or neglect. Elder abuse includes any
pattern of behavior that causes physical, psycho-
logical, sexual, fi nancial, or social harm to an
older person. The perpetrator often is a family
member (most commonly the spouse) or care-
History and examination of the injured eye
giver. The patient may appear withdrawn,
depressed, or anxious, and the caregiver may
give an inconsistent history. As with child abuse,
the physician should intervene with the aid of
the appropriate social services.7
RADIOLOGIC IMAGING
Several types of imaging studies are of great
utility following ocular and periocular trauma.
In general, these techniques should be employed
if the posterior pole is not adequately visualized
or if orbital fractures, optic canal impingement,
intraocular foreign bodies, or intraorbital foreign
bodies are suspected.
Plain radiography
With the advent of modalities such as computed
tomography (CT) and magnetic resonance
imaging (MRI), the use of plain radiography has
diminished significantly. However, it may be
employed when these other techniques are not
readily available.
Indications:
1. To determine the presence and location of
intraocular and intraorbital foreign bodies and
orbital fractures only when CT and MRI are
not available.
2. To screen for the presence of metallic foreign
bodies prior to MRI imaging.8
Advantages:
1. Readily available at most medical facilities.
2. Bony structures are visualized.
Disadvantages:
1. Does not detect radiolucent foreign bodies
(e.g. plastic, wood). 9
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
a ruptured globe include eyewall deformity
or wound, intraocular air, intraocular foreign
body, and intraocular hemorrhage.
2. To visualize the posterior segment when it is
not visualized on clinical examination and
ultrasonography is not available.
3. To determine the presence and location of
suspected intraocular or intraorbital foreign
bodies (Figure 3.11).
4. To determine the presence and location of
orbital fractures.
5. To determine the presence and location of
intracranial or intraorbital hemorrhage.
Advantages:
1. Readily available at most medical facilities.
2. No direct contact with the eyelids or globe is
necessary.
3. Visualizes both soft tissues and bony
structures.
4. Visualizes both radio-opaque (e.g. iron, glass,
graphite) and radiolucent foreign bodies with
excellent resolution capabilities.
Figure 3.11 A glass intraocular foreign body is readily
seen on this coronal computed tomography scan.
5. Visualizes fresh blood (without contrast
enhancement).
6. Can be performed on patients with suspected
or known metallic foreign bodies, those with
pacemakers, and those on life support.
7. Compared to MRI, CT is faster, less expen-
sive, produces less motion artifact, and is less
likely to induce claustrophobia.
Disadvantages:
1. May not be readily available if the patient
presents in an office-based setting.
2. Generally contraindicated in pregnant women
due to radiation exposure.
3. Resolution of intraocular structures is not as
high as ultrasonography.
4. Proper positioning for direct coronal scans
may not be possible for traumatized or unco-
operative patients. In these cases, coronal
reconstructions from axial images may be uti-
lized, but these images are of somewhat lower

34

quality than direct coronal images. Alterna-
tively, helical or spiral CT scanning can
provide better coronal images if this tech-
nique is available.11
Magnetic resonance imaging2,10
The role of magnetic resonance imaging (MRI)
in the setting of acute ocular and periocular
trauma is not well defi ned. MRI best visualizes
vascular lesions, intracranial processes, cavern-
ous sinus thrombosis, and inflammatory and
demyelinating optic nerve conditions.
Indications:
1. To visualize periocular soft tissues.
2. To visualize suspected vascular lesions, intra-
cranial pathology, and optic nerve lesions.
3. To locate non-magnetic intraocular or intra-
orbital foreign bodies.
Advantages:
1. Produces axial, coronal, and sagittal views
without repositioning the patient.
2. Soft tissue imaging is superior to that of CT.
3. Visualizes non-magnetic foreign bodies.
4. Can be used in pregnant women.
Disadvantages:
1. Not as widely available as CT.
2. Relatively long acquisition time, which can
produce motion artifact and claustrophobia.
3. Contraindicated in patients with suspected
magnetic intraocular or intraorbital foreign
bodies, pacemakers, cochlear implants, and
life support equipment.
4. Does not visualize bony structures as well as
CT.
Ultrasonography2,10
Of all of the imaging modalities discussed, ultra-
sonography (US) provides the greatest resolution
History and examination of the injured eye
and the most detailed anatomic information
regarding the posterior segment of the eye. It
has a resolution ranging from 0.1 to 0.01 mm.
Standard B-scan ultrasonography can visualize
radio-opaque and radiolucent intraocular foreign
bodies as well as pathology of the following
structures:
1. Vitreous (opacities, hemorrhage, posterior
vitreous detachment)
2. Retina (tears, detachment)
3. Choroid (serous choroidal detachment, supra-
choroidal hemorrhage, rupture)
4. Sclera (rupture).
It can also be used to visualize orbital structures
such as the lacrimal gland, extraocular muscles,
optic nerve, and orbital soft tissues. Ultrasound
biomicroscopy utilizes higher sound wave fre-
quencies to provide detailed images of the ante-
rior segment and its pathology, including occult
foreign bodies.12
Indications:
1. To evaluate the posterior segment when an
adequate view is not possible on clinical
examination.
2. To determine the presence and location of
intraocular (Figure 3.12) and intraorbital
foreign bodies.
Advantages:
1. Provides the highest resolution of intraocular
structures compared to CT and MRI.
2. Provides real-time cross-sectional and radial
views of the globe.
3. The equipment is relatively mobile, allowing
rapid imaging in a clinic setting, at the bedside,
or in the operating room.
Disadvantages:
1. Requires a trained and experienced techni-
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
 History and examination of the injured eye

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

38
 4
Definitions and classification
in ocular trauma
James T. Banta

INTRODUCTION ambiguity, especially between healthcare

Inherent difficulties will always exist in the eval-
uation of eye trauma. A seemingly white and
quiet eye can be rendered sightless from optic
nerve injury (i.e. traumatic optic neuropathy or
optic nerve avulsion) whereas an eye swollen
shut and diffusely hemorrhagic can appear dra-
matically damaged, yet quickly recover normal
vision. This is a primary reason for systemati-
cally approaching the evaluation of eye trauma
patients. Furthermore, defi ning a uniform termi-
nology and classification scheme for ocular
trauma is necessary to prevent confusion and
professionals.
The protean manifestations of ocular trauma
have long hobbled attempts at creating a mean-
ingful, clinically sound, and reproducible classifi-
cation system. Clearly, the ability to communicate
in a logical, formatted fashion is desirable, other-
wise collecting data and drawing comparisons
between similar groups becomes increasingly dif-
ficult. Likewise, communications between health
professionals is greatly hampered without a uni-
versally accepted vocabulary. Only in the last
decade, through the determined work of a few
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-
munication, particularly between healthcare
professionals. Never has this been more apparent
than with eye traumatology terms. Terms need
to be specific and unambiguous, both to expe-
dite appropriate diagnostic procedures and
referrals and, conversely, to avoid unnecessary
tests and consultations. Ruptured globe, open
globe, and globe laceration are often incorrectly
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
 Definitions and classification in ocular trauma

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?
Needless to say, this ambiguous terminology is
unacceptable.
STANDARD TERMINOLOGY
Once a unified set of defi nitions is available, a
coherent terminology system is possible. Created
simultaneously with the accepted defi nitions
described previously, the ocular traumatology
system,1–3 more recently revised as the Birming-
ham Eye Trauma Terminology (BETT),4 is a
simple yet comprehensive classification scheme
that removes ambiguity and redundancy. It has
been endorsed by the American Academy of
Ophthalmology, the International Society of
Ocular Trauma, the World Eye Injury Registry,
and the Vitreous and Retina Societies. Its
use is mandatory for publication in a multitude
of scientific journals (e.g. Ophthalmology,
Graefe’s Archive for Clinical and Experimental
Ophthalmology).
Figure 4.4 shows the pathway to making 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
 Definitions and classification in ocular trauma

always, ‘Is there a full-thickness defect of the
eyewall?’ If not, the closed globe injury is sepa-
rated into contusions (typically caused by a blunt
object) and lamellar lacerations (typically caused
by a sharp object). If a full-thickness defect
(open globe injury) is discovered, the next ques-
tion is ‘Was the injuring object, sharp or blunt?’
As discussed previously, a contusive force
introduced by a blunt object that induces a full-
thickness defect is a rupture. Conversely, a sharp
object that induces a full-thickness defect is a
laceration, but needs further distinction. Three
possibilities exist:
1. The entry and exit wound is the same: pene-
trating injury (Figure 4.3A).
2. Separate entry and exit wounds caused by the
same object are present: perforating injury
(Figure 4.3B).
3. An entry wound is present and the object (or
a portion thereof) remains within the eye:
intraocular foreign body (Figure 4.3C).
By using the eyewall as the frame of reference,
confusion is limited. For example, a penetrating
scleral wound refers to an entry into but not
through the sclera. This would be a closed globe
injury (lamellar laceration by BETT), but could
easily be mistaken for an open globe injury. Con-
versely, a perforating scleral wound implies an
entry into and through the sclera. However, since
the eyewall is not used as a frame of reference
one cannot tell whether a globe laceration or an
IOFB is present. This could easily be a source of
confusion and misunderstanding that can lead to
further miscommunication between healthcare
professionals and to inappropriate or unneces-
sary evaluations. However, when the eyewall is
used, this confusing situation is avoided and
tissue-specific terms are used only to locate the
entry wounds.

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
sometimes are referred to as mixed-mechanism
injuries. Nevertheless, these exceptions aside,
the vast majority of injuries can be easily classi-
fied and related to other healthcare professionals
in a uniform fashion.
CLASSIFICATION
4.2) and closed (Table 4.3) globe injuries. Injuries
due to chemical, thermal, or electrical agents are
not included in the classification. A recent study
showed that all four variables were significant in
predicting fi nal visual outcome following open
globe injury, although grade (visual acuity) and
pupil (presence of a relative afferent pupillary
defect) were the most significantly predictive.5

A clinical classification system for mechanical PROGNOSIS AND PREOPERATIVE

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

46
 Definitions and classification in ocular trauma

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
makes for a difficult situation. A question that
often occurs is ‘Will I go blind?’ or ‘Will my
vision recover?’
Being able to give a logical, scientifically based
prognostication based on the initial examination
allows the physician to counsel a patient and the
patient’s family objectively. Numerous studies
have examined factors influencing fi nal visual
acuity following severe ocular trauma.6–8 Poor
preoperative visual acuity, presence of a relative
afferent pupillary defect, retinal detachment,
and large scleral lacerations were found to be
poor prognostic indicators for fi nal visual acuity
outcomes. In the largest study to date, Kuhn
et al in 20029 analyzed over 2500 eye injuries.
Through statistical analysis, six variables were
found to be of prognostic significance, and each
variable was then assigned a point value (Table
4.4). The mathematical sum of the given vari-
ables is then broken into five categories (Table
4.5) and allows the physician to estimate the
given probability of a certain level of visual
acuity recovery. This system is referred to as the
Ocular Trauma Score (OTS) and can be posted
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
is long and fraught with multiple surgeries and
possible complications. Never downplay the sever-
ity of the injury or the possibility for permanent loss
of sight. Be realistic when discussing the progno-
sis of the severely injured eye while maintaining
guarded optimism.
Anger and sadness are common reactions in
the patient with a severely injured eye. Honesty
and straightforward communication fosters a

48

trust between the patient and physician. Insist
the patient be involved in the decision-making
process. The Ocular Trauma Score is a spring-
board for answering difficult questions, but per-
sonal experience and common sense should
facilitate an honest conversation and a good rela-
tionship between patient and physician. My per-
sonal experience has been that these patients are
often some of the most loyal and grateful patients,
even when their visual outcomes are poor. If the
patient realizes that all steps are being made to
restore vision, their reaction to the physician and
ancillary staff is typically one of gratitude,
although their reaction to the situation may
often remain negative.
SUMMARY
1. Strict adherence to the accepted ocular
traumatology defi nitions (Birmingham Eye
Trauma Terminology or BETT) is vital when
assessing patients with eye injuries and when
relaying information to eye care professionals.
Only when these components are fully inte-
grated into the vocabularies and methodo-
logies of physicians caring for this population
of patients can effective communication and
reliable triage of patients be accomplished.
2. Establishing an honest, therapeutic relation-
ship with the patient is of utmost importance
when facing a severe ocular injury. Involve the
patient in the decision-making process and
Definitions and classification in ocular trauma
assure them all steps are being taken to restore
sight.
REFERENCES
1. Kuhn F, Morris R, Witherspoon CD, Heimann K, Jeffers JB,
Treister G. A standardized classification of ocular trauma.
Ophthalmology 1996;103:240–243.
2. Kuhn F, Morris R, Witherspoon CD, Heimann K, Jeffers JB,
Treister G. A standardized classification of ocular trauma.
Graefe’s Arch Clin Exp Ophthalmol 1996;234:399–403.
3. Pieramici DJ, Sternberg P Jr., Aaberg TM Sr., et al. A system of
classifying mechanical injuries of the eye (globe). Am J
Ophthalmol 1997;123:820–831.
4. Kuhn F, Morris R, Witherspoon CD. Birmingham Eye Trauma
Terminology (BETT): terminology and classification of
mechanical eye injuries. Ophthalmol Clin North Am
2002;15(2):139–143.
5. Pieramici DJ, Au Eong KG, Sternberg P Jr., Marsh MJ.
The prognostic significance of a system for classifying
mechanical injuries of the eye (globe) in open-globe
injuries. Journal of Trauma-Injury, Infection and Critical
Care 2003;54:750–754.
6. Hutton WL, Guller DG. Factors influencing final visual
results in severely injured eyes. Am J Ophthalmol 1984;97:
715–722.
7. Abu El-Asrar AM, Al-Amro SA, Khan NM, Dangave D. Visual
outcome and prognostic factors after vitrectomy for
posterior segment foreign bodies. Eur J Ophthalmol
2000;10:304–311.
8. De Souza S, Howcroft MJ. Management of posterior segment
intraocular foreign bodies: 14 years’ experience. Can J
Ophthalmol 1999;34:23–29.
9. Kuhn F, Maisiak R, Mann L, Mester V, Morris R, Witherspoon
CD. The Ocular Trauma Score. Ophthalmol Clin N Am
2002;15:163–165.
49

Closed globe injuries: ocular surface
(conjunctiva, cornea, and sclera)
Kristen L. Hartley, Benjamin L. Mason, James T. Banta
INTRODUCTION
Closed globe injuries to the conjunctiva, sclera,
and cornea are commonplace and are a frequent
reason emergency ocular care is sought. When
the eyes are open, the ocular surface (particu-
larly the epithelium of the cornea and conjunc-
tiva) acts as a protective barrier to the elements.
The majority of ocular surface injuries occur
when a foreign substance or object inadvertently
(job-related accident) or purposefully (assault)
comes into contact with the ocular surface.
Depending on the mechanism of injury, these
injuries vary from mild (subconjunctival hemor-
rhage) to vision threatening (alkali exposure).
While most surface injuries are benign and
resolve without intervention, others require close
inspection and prompt treatment to prevent per-
manent dysfunction or late complications. Com-
placency is ill advised as a seemingly innocuous
injury can sometimes herald more serious pathol-
ogy. A comprehensive examination is necessary
for even a seemingly minor injury. In this chapter
we will review common traumatic injuries to the
ocular surface.
EVALUATION: GENERAL
CONSIDERATIONS
Injuries to the ocular surface encompass a vast
array of diagnoses. Although the specific history
and examination fi ndings for each diagnostic
entity will be described individually, the evalua-
tion for injuries of the ocular surface should
5
proceed in a stepwise fashion. History is critical
in determining the mechanism of injury. In par-
ticular, the patient’s activities at the time of
injury, the injuring agent, subsequent vision loss,
prior treatments, and current level of discomfort
should be thoroughly documented. However,
thorough history taking in the setting of chemi-
cal injuries should initially be avoided so that
immediate and copious irrigation of the eye can
begin.
The upper and lower conjunctival fornices are
formed at the transition between tarsal and
bulbar conjunctiva (Figure 5.1). The fornices can
harbor unrealized foreign material or retained
chemicals. The upper lid should be everted to
examine the tarsal conjunctiva and, in appropri-
ate cases, ‘double eversion’ of the eyelid is per-
formed to thoroughly examine the upper fornix
(see Chapter 3).
The ocular examination will vary depending
on the mechanism of injury. An initial inspec-
tion is made to ascertain the integrity of the
eyewall. Once an open globe injury has been
excluded, a thorough examination of the ante-
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
and bulbar conjunctiva should be examined for
presence of hemorrhage, foreign material, edema,
subconjunctival air, or lacerations. The cornea
should be examined for the presence of epithe-
lial defects, foreign bodies, lamellar lacerations,
or limbal stem cell ischemia. The sclera should
also be examined for lamellar lacerations, foreign
bodies, and structural integrity.
51
 Ocular trauma
Superior
conjunctival
fornix
Inferior
conjunctival
fornix
Figure 5.1 The tarsal conjunctiva (red) begins at the
posterior edge of the eyelid margin and is tightly
adherent to the underlying tarsal plate. The palpebral
conjunctiva (blue) inserts at the limbus, is more mobile
and overlies Tenon’s capsule. The superior and inferior
conjunctival fornices form at the transition between
the tarsal and palpebral conjunctiva.
TRAUMATIC SUBCONJUNCTIVAL
HEMORRHAGE
Introduction
Subconjunctival hemorrhage is a very common
condition that presents as an ocular emergency,
in large part due to its often dramatic appear-
ance. The causes of subconjunctival hemorrhages
are numerous and the severity can be variable.
Spontaneous subconjunctival hemorrhage is
frequently due to Valsalva maneuvers that raise
venous pressure such as coughing, sneezing,
vomiting, or heavy lifting. Acute bacterial or
52
Figure 5.2 Subconjunctival hemorrhage associated
with an open globe is often present 360 degrees and
associated with chemosis. This 42-year-old female
suffered a severe contusive trauma to the left eye and
was found to have a large posterior rupture during
surgical exploration.
viral conjunctivitis is also a common cause. Sys-
temic hypertension and anticoagulation can pre-
dispose patients to more frequent hemorrhages.1,2
Frequently, no specific cause is elucidated.
Traumatic subconjunctival hemorrhage can be
related to trauma as minor as excessive eye
rubbing or as extreme as open globe injuries.
Evaluation
History is the most important step in determin-
ing the etiology of a subconjunctival hemorrhage.
Subconjunctival hemorrhage often obscures the
underlying sclera so eliciting the exact mecha-
nism of injury can help the examiner determine
the risk of severe ocular damage. Occult globe
violation can be masked by the presence of dense
subconjunctival hemorrhage and requires a high
index of suspicion to diagnose (Figure 5.2).
Careful examination technique can typically
detect the presence or absence of an occult globe
violation in the setting of dense subconjunctival
hemorrhage. Examination clues include:
 Closed globe injuries: ocular surface (conjunctiva, cornea, and sclera)
1. peaked pupil
2. asymmetric anterior chamber depth
3. asymmetrically low intraocular pressure
4. subconjunctival pigment
Chapter 11 explores the diagnosis of occult globe
violation in further detail.
Treatment
Recognizing and treating any associated ocular
injuries is the fi rst and most important step. The
only treatment for subconjunctival hemorrhage
is time. Most subconjunctival hemorrhages
resolve in a matter of days but can take several
weeks if extensive. Conservative measures
such as lubricant eye drops and reassurance are
satisfactory with isolated subconjunctival
hemorrhages.
Patients with isolated subconjunctival hemor-
rhages can be followed on an as-needed basis
assuming a routine recovery. Patients need to be
informed that the hemorrhage can initially
expand in size and eventually change color over
a 10–14-day course. If significant trauma led to
the hemorrhage then follow-up is determined by
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
Patients typically present with intense pain, pho-
tophobia and redness. Careful questioning about
the mechanism of injury is important as it helps
determine the risk of infection or retained foreign
body.
A corneal abrasion can be hard to see at the slit
lamp unless the loose epithelium is heaped up
and incompletely avulsed from the underlying
stroma. Fluorescein staining of the cornea is the
mainstay of diagnosis. When the epithelial defect
is stained, the affected area can easily be visual-
ized and measured. The areas without epithe-
lium take up the fluorescein and turn bright
green under examination with a cobalt blue fi lter
(Figure 5.3). Documenting the horizontal and
vertical size of the defect can be helpful in moni-
toring a patient’s recovery.
Associated exam fi ndings may include subcon-
junctival hemorrhage, conjunctival abrasions and
lacerations, corneal stromal edema, Descemet’s
folds (Figure 5.4), and anterior chamber cell and
flare. With very severe trauma a corneal abrasion
may be seen with hyphema, commotio retinae,
or even an open globe.
Further exam is critical to rule out associated
conditions that can coexist with corneal
Figure 5.3 A defect in the corneal epithelium is most
easily observed utilizing fluorescein dye viewed with a
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
 Closed globe injuries: ocular surface (conjunctiva, cornea, and sclera)
Figure 5.6 As the corneal epithelium heals, a pseudo-
dendritic appearance is sometimes seen in the final
stages of healing.
if a partially avulsed flap of corneal epithelium
can be temporarily replaced this should be
avoided. With repeated blinking the loose epi-
thelium will again become dislodged and may
hinder the healing process and contribute to
patient discomfort. A moistened sterile swab can
be used to debride a partially avulsed epithelial
flap, but use of a sharp blade to remove heaped-
up edges or large sheets of loose epithelium is
preferred as it is less likely to propagate the
defect into normal epithelium.
One of the keys to treatment success is removal
of any residual foreign material. The upper lid
should be everted and the tarsal conjunctiva
should be examined for foreign bodies. The
conjunctival fornices should be swept if the
potential for foreign material exists. This is ac-
complished after applying topical anesthetic to
the eye. A moistened cotton swab or glass rod is
introduced into the conjunctival fornix (both
superior and inferior) and is moved along the
entire length of the forniceal space. If debris is
encountered, the procedure should be repeated
until no foreign material is seen. Corneal or con-
junctival foreign bodies should likewise be
removed (see below).
Prophylactic broad-spectrum antibiotics and
observation are the mainstays of treatment for
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.
Studies have shown that occlusive patching does
not significantly speed corneal re-epithelializa-
tion or improve patient comfort.6,7 Furthermore,
the fear of possibly accelerating infection has
tempered the use of patching in recent years. In
the absence of apparent infection, the authors
prefer to utilize an antibiotic ointment (bacitra-
cin or erythromycin ointment) without occlusive
patching. In the rare instances we use occlusive
patches, we patch only if the wound is consid-
ered low risk (no history of contact lens use or
exposure to organic material) and pain is seem-
ingly uncontrollable. This is only done if the
patient is deemed reliable and agrees to follow-
up the following day. Never patch an eye that has
an abrasion associated with contact lenses or
organic material.
In the presence of a suspected infectious kera-
titis, corneal scrapings are obtained and sent for
Gram stain and culture. Our initial antibiotic
choice depends on the location and size of the
infi ltrate. For a small peripheral infi ltrate, the
authors prefer a fourth-generation fluoroquino-
lone used hourly. If the infi ltrate is large or
threatening the visual axis, fortified cefazolin
and tobramycin are prescribed and used hourly.
Antibiotic use is then tailored to the culture
results.
Pain is a significant issue with corneal abra-
sions. Fortunately, in routine cases, the rapidity
with which the corneal epithelium regenerates
55
 Ocular trauma
causes the painful episode to be relatively short-
lived. Abrasions located within the intrapal-
pebral space are more symptomatic as blinking
causes contact with the injured epithelium. Con-
versely, abrasions located in the superior aspects
of the cornea tend to be better tolerated since
the upper lid covers and protects them. We rou-
tinely counsel patients on the expected discom-
fort as the abrasion heals. If the abrasion is small
or the patient is pain-tolerant, acetaminophen
taken regularly during the acute phase is recom-
mended. Acetaminophen should be avoided in
patients with liver dysfunction and recom-
mended dosages should be followed closely. If
the patient is in severe pain, as is often the case,
a prescription for a 2-day supply of narcotic anal-
gesics is given.
Complications and outcomes
Patients who are patched should be examined
within 24 hours. Non-patched small abrasions
can be given antibiotic coverage for 3–5 days
with follow-up scheduled on an as-needed basis.
For large abrasions the healing process should be
evaluated in 1–2 days. If signs of infection are
present or if the abrasion is considered high risk
for infection, daily follow-up is warranted until
healing is complete.
Changes in corneal epithelial adherence can
occur following a traumatic corneal abrasion.
This can lead to recurrent corneal erosions in the
absence of significant trauma.4 These patients
often report a history of waking from sleep with
severe eye pain that may resolve over the next
few hours. If the problem is recalcitrant despite
appropriate lubricant use, referral to an anterior
segment specialist is warranted, as various thera-
peutic modalities are available (stromal punc-
ture, therapeutic keratectomy).
The use and abuse of anesthetic drops deserves
special mention. The pain from corneal abra-
sions can be intense. The placement of a topical
56
anesthetic drop gives a ‘miraculous’ reprieve
from the pain often leaving the patient incredu-
lous when they are told it cannot be used rou-
tinely. Chronic use of topical anesthetics retards
wound healing and can lead to severe corneal
complications such as corneal melting.8 The
authors have seen patients attempt to steal
topical anesthetic bottles from the examination
room. We have also seen topical anesthetics inap-
propriately prescribed by non-ophthalmologists.
Healthcare providers (including veterinarians)
are a high-risk group for anesthetic abuse since
they often have access to the medicines but are
not always aware of its associated dangers. Spe-
cific counseling as to why the anesthetic drops
are not a part of treatment is recommended, and
anesthetic bottles need to be accounted for at the
end of each examination. Deterioration of the
cornea following a corneal abrasion should spur
an inquiry about the inappropriate use of topical
anesthetics.
CORNEAL FOREIGN BODIES
Introduction
Corneal foreign bodies are one of the most
common forms of ocular trauma, second only to
corneal abrasions.9 It is of utmost importance
that each patient presenting with a corneal
foreign body be educated on the use of protec-
tive eyewear, as this could prevent most com-
monly encountered corneal foreign body injuries
(see Chapter 2). Most corneal foreign bodies are
not associated with a high level of morbidity, but
it is essential to perform a thorough examina-
tion, including a dilated fundus examination, to
rule out an intraocular foreign body.
Etiology
The causes of corneal foreign body injuries are
numerous. Injury may occur to the unassuming
individual who has debris blown into the eye
 Closed globe injuries: ocular surface (conjunctiva, cornea, and sclera)
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
history will lower (e.g. something fell into the
eye while walking down the street) or raise
(e.g. hammering metal on metal) the suspicion
of a more serious injury. After obtaining a history,
full ophthalmic examination should be per-
formed. Visual acuity is an essential piece of
information and if decreased should raise the
suspicion for a more serious injury. An initial
screening slit lamp examination should be per-
formed to confi rm that no globe violation has
occurred. Carefully document intraocular pres-
sure in both the affected and unaffected eye.
Asymmetric intraocular pressure readings may
be an early clue that the integrity of the globe
has been compromised. Full slit lamp examina-
tion should begin with evaluation of the patient’s
lids and lashes. Evert the upper lids and evaluate
both the upper and lower tarsal conjunctiva and
fornices for any evidence of retained foreign
bodies. Vertically oriented linear corneal abra-
sions often coexist with subtarsal foreign bodies
and are easily seen with fluorescein staining.
Conjunctival chemosis should raise the suspicion
for a globe violation if present. The bulbar con-
junctiva should be thoroughly inspected for lac-
erations, foreign bodies, or debris.
Often a corneal foreign body is quite obvious
(Figure 5.7). It is of paramount importance to
continue looking for other foreign bodies or con-
comitant ocular injuries even when an obvious
Figure 5.7 A metallic corneal foreign body is
embedded in the nasal aspect of the cornea in a 26-
year-old male patient who suffered the injury while
grinding metal without appropriate eye protection.
foreign body is present. The cornea should fi rst
be evaluated with a wide beam and then a slit
beam to determine the depth of a corneal foreign
body. The location and properties (metallic or
non-metallic) of the foreign body should be doc-
umented. If the foreign body is in the posterior
portion of the corneal stroma, perform a Seidel
test over the area of the foreign body before and
after removal to rule out egress of aqueous from
the wound. The anterior chamber should be
evaluated thoroughly, including depth of the
chamber, amount of anterior chamber reaction,
and evidence of hyphema or hypopyon. The iris
should be evaluated for the presence of trans-
illumination defects and the lens for evidence
of anterior lens capsule disruption, intralenticu-
lar foreign body, or cataractous changes. Finally,
a dilated fundoscopic examination should be
performed if an intraocular foreign body is a
possibility.
Treatment
Most corneal foreign bodies are metal and can
be removed easily at the slit lamp. Shallow
foreign bodies often can be dislodged with a
57
 Ocular trauma
moistened sterile cotton swab. Embedded foreign
bodies can be removed with a small gauge needle
(27- or 30-gauge), ophthalmic ‘spud,’ rotating
ophthalmic burr, or a combination of the three.
In the case of a metallic foreign body, it is impor-
tant to remove any associated rust ring to prevent
a secondary keratitis. The following steps are
used when removing a corneal foreign body:
1. Anesthetize the eye.
2. Insert a lid speculum (if the patient has diffi-
culty keeping the eye open).
3. Place the patient in the slit lamp and locate
the foreign body (Figure 5.8A).
4. Using a needle, approach the cornea tangen-
Included
tially so that no sudden movement could lead
on DVD
to perforation of the anterior chamber.
5. Gently dislodge the foreign body and remove
it from the surface of the eye (Figure 5.8B).
6. If metallic, the foreign body typically leaves a
rust ring in place which is removed with an
ophthalmic corneal burr (Figure 5.8C) until
the ring is entirely removed (Figure 5.8D).
7. After the foreign body has been removed, the
patient should be placed on an antibiotic oint-
ment (e.g., bacitracin or erythromycin) four
times daily and a cycloplegic, if necessary.
8. Counseling on the necessity for protective
safety goggles during high-risk activities is
vital as recurrences are common with metallic
corneal foreign bodies.
Deeply embedded foreign bodies can be quite
challenging to manage. When the foreign body
is greater than 80% depth, it is possible that
removal may create a small full-thickness corneal
injury. If removal is attempted, a Seidel test
should be performed immediately afterwards. If
positive, a decision to use corneal glue or a suture
will need to be made. Most small-caliber wound
leaks following foreign body removal will close
spontaneously in a matter of hours and can be
closely observed with the typical regimen of
topical antibiotics and a protective shield over
58
the eye to prevent inadvertent eye rubbing. A
topical aqueous suppressant is sometimes pre-
scribed to decrease the flow of aqueous through
the wound thereby encouraging wound healing.
Daily follow-up is mandatory in these cases.
Deep foreign bodies consisting of an inert
substance (e.g. glass, plastic) are sometimes
left in place to be serially observed. Foreign
bodies will sometimes slowly migrate anteriorly
with time allowing for a safer, more controlled
removal.
Complications and outcomes
Follow-up should be tailored to each individual
patient. If the corneal foreign body is small and
leaves only a small corneal epithelial defect and
no rust ring after removal, the patient may be
seen on an as-needed basis. In the case of a large
corneal foreign body with a large epithelial defect
after foreign body removal, the patient should be
followed daily to be sure the abrasion is healing
with no evidence of secondary infection. If a rust
ring is still present at discharge, the patient
should be followed daily with continued attempts
to remove all rust from the cornea. In many
cases, the rust is more easily removed after 1–2
days of observation. All patients should be
instructed to return immediately if symptoms
worsen (e.g. decreased vision, increased pain or
redness).
CHEMICAL INJURIES
Introduction
Chemical injuries are true ocular emergencies.
Every second counts after a chemical injury since
the amount of tissue damage is directly related
to the length of time the chemical remains in
contact with the eye. Immediate irrigation is
vital. Ideally, irrigation should begin long before
a patient’s presentation to the emergency room.
 Closed globe injuries: ocular surface (conjunctiva, cornea, and sclera)

A B

C D

Figure 5.8A–D Metallic corneal foreign body removal.

Chemical composition is also important. Alka-
line agents tend to penetrate the eye more readily
than acids thereby carrying a significantly higher
morbidity.10–12
Depending on the depth of ocular penetration,
a chemical injury may cause damage to many
ocular structures including the corneal and
conjunctival epithelium, basement membrane,
corneal stroma and endothelium, lens epithe-
lium, and vascular endothelium of the conjunc-
tiva, episclera, iris, and ciliary body.11 Penetration
into the anterior chamber may occur rapidly
after some alkali injuries (e.g. ammonia), further
emphasizing the importance of immediate treat-
ment.10–12 Education, particularly for high-risk
individuals such as custodians and laboratory
workers, is very important because they need to
be aware that irrigation should be started at
home or in the field immediately after exposure.
Prevention with appropriate eye protection could
prevent most, if not all, chemical injuries in
working environments.

59
 Ocular trauma
Figure 5.9 Diffuse conjunctival ischemia, corneal haze,
and a sterile inflammatory hypopyon are seen
following a severe alkali exposure.
Pathophysiology
As stated previously, chemical injuries may be
associated with either acid or alkali compounds.
Alkalis cause the most severe damage by dis-
rupting the corneal barrier and allowing rapid
passage into more posterior ocular structures.
Lye (NaOH, KOH), fresh lime (CaO, found in
plaster and concrete), and ammonia are the most
commonly involved agents.10,11 Alkalis result in a
more severe injury as they rapidly penetrate the
eye, saponify cell membranes, denature collagen,
and thrombose vessels (Figure 5.9).12 Intraocular
pressure may be elevated initially due to shrink-
age of the scleral collagen and later by sclerosis
of the aqueous outflow channels.11–13 Acids gen-
erally cause less damage because the hydrogen
ion precipitates protein and prevents further
penetration through the cornea (Figure 5.10).12
However, treatment and potential complications
are similar for both alkali and acid injuries.
Evaluation
Obtaining an initial history of chemical expo-
sure is all that is necessary before immediate,
copious irrigation with liter bags of normal saline
is initiated. The eye should be irrigated with
normal saline until the pH of the eye normalizes
60
Figure 5.10 Moderate conjunctival injection with a
central corneal epithelial defect following exposure to
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.
(Figure 5.11).11 This can be an arduous, messy
process that can sometimes take over an hour,
but it is essential to minimize further damage to
the eye.10,13,14 To achieve complete irrigation of
the conjunctival fornices, it is often necessary
to apply topical anesthetic (e.g. tetracaine or
proparacaine) and retract the lids with a lid
speculum or Desmarres retractor.15 Irrigation is
complete when the pH of the eye has normalized
and all foreign material has been removed. While
irrigation is being performed, a thorough history
should be obtained to determine the type of
chemical involved. If a sample of the chemical is
available, pH testing should be performed
directly on the sample.
Once irrigation is complete, a more compre-
hensive examination is performed. Vision and
pressure should be documented, as the pressure
may be acutely elevated. Attention is then focused
on the anterior segment. The lids and lashes are
evaluated to look for any evidence of crystallized
chemicals. These are removed immediately if
present. The upper and lower conjunctival for-
nices should be swept with a glass rod or sterile
cotton swab to remove any offending agents.
A careful examination of the conjunctiva and
 Closed globe injuries: ocular surface (conjunctiva, cornea, and sclera)
Figure 5.11 Following a chemical injury, immediate
copious irrigation of the involved eye is initiated with
liter bags of normal saline.
cornea should be performed. The Roper-Hall
modification of the Hughes classification system
is a widely accepted guide for the standardized
assessment and prognosis of chemical burns:16
1. Grade 1: epithelial damage with no limbal
ischemia
2. Grade 2: corneal haze, visible iris details, and
ischemia less than one-third of the limbus
3. Grade 3: total loss of corneal epithelium,
stromal haze obscuring iris details, and is-
chemia of one-third to one-half of the limbus
4. Grade 4: opacified cornea, iris and pupil
obscured, and ischemia involving more than
half of the limbus.
The size of the corneal epithelial defect should
be well documented as well as the clock hours
of limbal ischemia, if present. Limbal ischemia
appears as a blanching of normal limbal vessels
(Figure 5.12). A white eye in the setting of a
chemical injury is a very poor prognostic indica-
tor and indicates diffuse vascular damage. Ante-
rior chamber reaction should be documented as
this can provide indirect evidence of intraocular
chemical penetration.
Figure 5.12 Severe conjunctival and limbal ischemia
following an alkali injury. Notice the pruning of the
remaining conjunctival vessels.
Treatment
Initial management, as mentioned previously,
involves copious irrigation and meticulous
removal of all chemical residues. Irrigation is
typically performed with the patient lying at an
angle, allowing the excess water to be collected
in a basin. Retractors are used to make certain
the fluid reaches the conjunctival fornices. This
is continued until the pH of the eye normalizes.
Successful long-term management of chemical
burns involves promoting re-epithelialization,
minimizing inflammation, and reducing the inci-
dence of corneal perforation. The management
of chemical injuries is dependent on the degree
of ocular injury. In the case of a Grade 1 injury,
the patient should be treated with an antibiotic
ointment (e.g. bacitracin or erythromycin) four
times daily to the affected eye and a cycloplegic
(e.g. scopolamine) to decrease ciliary spasm and
decrease the formation of posterior synechiae.12
One can also consider the use of topical steroids
(e.g. prednisolone acetate) to decrease the
inflammatory response for the fi rst 7–10 days
after injury.11–14 Topical steroids should be rapidly
61
 Ocular trauma
tapered after that time due to the risk of impaired
wound healing with long-term use. In more
severe injuries, high-dose vitamin C (500 mg
orally four times a day), 10% ascorbate drops
every 2 hours, and 10% citrate drops every 2
hours were associated with a more rapid recov-
ery and better fi nal visual outcome in one study.17
Oral doxycycline (50–100 mg orally two times
a day) is a potent inhibitor of collagenase and
may reduce the risk of corneal perforation in a
severely injured eye.18
Intraocular pressure in a chemically injured eye
may be high or low. Decreased pressure is usually
due to ciliary body damage. A high IOP is most
likely caused by collagen shrinkage or inflam-
matory debris obstructing the trabecular mesh-
work.11–13 Control of IOP is best achieved with
aqueous suppressants, such as topical beta-
adrenergic antagonists (e.g. timolol), alpha-
CASE EXAMPLES
Case report: chemical injury (Figure 5.13)
A 48-year-old male was working when a car battery
(sulfuric acid) exploded in his face. He immediately
flushed the eyes with water but noted severe
decrease in visual acuity associated with severe pain
in both eyes. Initial visual acuity was counting fingers
in both eyes. Slit lamp examination of the right eye
revealed extensive conjunctival ischemia with limbal
vessels present only superiorly. Extensive superficial
necrosis and white blood cell infiltration of the
cornea obscured the view of anterior chamber struc-
tures, although the anterior chamber did appear to
be formed (A). The left eye suffered only a small
central epithelial defect and will not be discussed
further. The patient was started on an antibiotic oint-
ment, cycloplegic drops, and topical steroids. He
62
adrenergic agonists (e.g. brimonidine), or carbonic
anhydrase inhibitors (e.g. dorzolamide).11–13
Complications and outcomes
The patient should be followed on a daily basis
to ensure the treatment regimen is leading to
clinical improvement. In severe cases with limbal
ischemia or intraocular complications, daily
visits are essential to monitor for evidence of
corneal thinning or perforation. Rarely, immedi-
ate surgical treatment with a temporary tarsor-
rhaphy, corneal glue, or if these more conservative
measures fail, an emergent corneal patch graft or
corneal transplant is necessary when perforation
occurs or is imminent. Consultation with an
anterior segment specialist is often necessary for
long-term management, particularly when limbal
stem cell ischemia is present and/or anterior
segment reconstruction is necessary.
returned 3 days later with reports of improved
comfort and vision. Visual acuity improved to 20/60.
Slit lamp examination revealed a central clear
zone devoid of epithelium. The peripheral cornea
remained opaque with significant white blood cell
infiltrate (B). Treatment was continued and the
patient slowly improved. Follow-up 17 days after the
initial injury showed dramatic improvement in con-
junctival vascularization associated with clearing
and re-epithelialization of the peripheral cornea. A
small central epithelial defect persisted (C). Four
weeks after the initial injury, the cornea was com-
pletely re-epithelialized with a mild anterior stromal
haze (D). Best corrected visual acuity was 20/50.
 Closed globe injuries: ocular surface (conjunctiva, cornea, and sclera)

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-
tion and tearing. A history consistent with a
foreign body injury such as inadvertently being
poked in the eye is typically elucidated. The
nature of the injury can help one develop an
in the eye while playing basketball. A stellate, 12 mm
conjunctival laceration was present temporally. Since
the laceration was largely protected by the lids, the
patient experienced minimal discomfort and the
laceration healed without suturing.

63
 Ocular trauma
initial assessment of the patient’s risk of globe
violation and infection.
Examination should consist of a complete
ocular examination including a dilated fundus
examination to rule out a more serious injury.
Special attention is given to the area of the lac-
eration. Fluorescein can help determine the size
of the laceration. If the underlying sclera is lacer-
ated, a Seidel test should be performed at the
site to rule out an open globe injury (see Chapter
3). Every conjunctival laceration should be
explored extensively under topical anesthesia.
The length of laceration, the approximation of
the wound edges, and the amount of debris
should be documented. Conjunctival chemosis
and surrounding subconjunctival hemorrhage
can sometimes obscure foreign material and
scleral injury, so gentle probing with a cotton
swab can be useful under topical anesthesia.
Retained foreign bodies can increase a patient’s
risk of infection and persistent inflammation.
Rarely, pigmented uvea protruding through a
full-thickness scleral laceration can be confused
with a foreign body and requires careful exami-
nation under a slit lamp to help differentiate
between the two entities.
Treatment
Once the integrity of the eyewall is confi rmed,
cotton swabs, forceps, or saline irrigation can be
used to remove persistent debris or residual
chemical residue. Most small conjunctival lacera-
tions can be treated conservatively with prophy-
lactic topical antibiotics for 5–7 days. Antibiotic
ointments are often utilized as their lubricating
properties contribute to the patient’s comfort,
although topical drops will suffice.
Some ophthalmologists advocate suturing all
conjunctival lacerations. Most small lacerations
(<10 mm) will heal quickly without surgical
intervention. Larger (>10 mm), poorly approxi-
mated, and horizontally oriented conjunctival
64
lacerations should often be sutured. A horizon-
tally oriented laceration often comes in contact
with the lid margin during blinking, thus pro-
longing healing time and increasing foreign body
sensation. Large and/or poorly approximated
wounds will often eventually heal without inter-
vention but can leave scar tissue and produce a
chronic foreign body sensation. Absorbable
suture such as polyglactic acid (7-0 or 8-0)
should suffice to cover bare sclera and can be
done in a minor operating room or even at the
slit lamp. The authors prefer to close large con-
junctival lacerations if the approximation is poor
and healing is likely to cause scarring if left unsu-
tured. We employ multiple buried simple inter-
rupted sutures to assure good closure and
decrease the risk of wound dehiscence if a suture
breaks.
Complications and outcomes
Isolated small lacerations treated only with pro-
phylactic antibiotics can be seen on an as-needed
basis if their recovery is unremarkable. More
extensive or sutured lacerations should be re-
evaluated in 5–7 days.
LAMELLAR CORNEAL AND
SCLERAL LACERATIONS
Introduction
Lamellar or partial-thickness lacerations of the
cornea and sclera are relatively uncommon (aside
from metallic corneal foreign bodies discussed
earlier). These injuries are often caused by
foreign body trauma with a sharp object such as
a screwdriver or pencil (Figure 5.15).
Evaluation
History is critical, particularly the mechanism of
injury. The injuring object should be identified,
 Closed globe injuries: ocular surface (conjunctiva, cornea, and sclera)
A from the laceration site can sometimes reveal
B resistant to topical antibiotics. For this reason
Figure 5.15 A 42-year-old male was struck with a tile
fragment while cutting tiles without appropriate eye
protection. A horizontally oriented corneal laceration
was noted (A). Slit beam examination revealed the
laceration was approximately 80% depth (B). A Seidel
test was negative. A shield was placed over the eye and
the patient was placed on prophylactic antibiotic
drops. Serial observation was elected, and the wound
healed without sequelae.
if possible. A thorough examination of the
injured area is then performed to confi rm that
the wound is indeed only partial thickness. A
Seidel test is of utmost importance. If a wound
is considered highly suspicious yet has an ini-
tially negative test, light globe pressure away
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
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.
Complications and outcomes
Deep lamellar lacerations should be followed
closely for signs of infection and to ensure wound
healing is adequate. Patients should be given spe-
cific instructions about the symptoms of infec-
tion and instructed to return immediately if such
symptoms occur. Depending on the location and
depth of the wound, lamellar corneal lacerations
often leave a scar and can sometimes induce
irregular astigmatism.
SUMMARY
1. Injury to the ocular surface (particularly
corneal abrasion) is the most commonly
65
 Ocular trauma
encountered sequela following ocular
trauma.
2. Appropriate eye protection could prevent all
on-the-job ocular surface injuries.
3. Traumatic subconjunctival hemorrhage has no
specific treatment, but should lead to an
appropriate examination to rule out concomi-
tant ocular injury.
4. Corneal abrasions typically heal quickly and
require only prophylactic antibiotics. Loose
sheets of epithelium should be debrided to
promote re-epithelialization.
5. Metallic corneal foreign bodies and their asso-
ciated rust rings should be completely removed
to prevent keratitis. Occasionally, recalcitrant
rust rings are left in place for 1–2 days (while
using a prophylactic antibiotic) since delayed
removal is often much easier to accomplish.
6. Irrigation of chemical injuries should begin
before the patient arrives in the emergency
room and again upon arrival at the emergency
room. Irrigation should continue until the pH
of the eye normalizes.
7. Small well-approximated conjunctival lacera-
tions often heal without suturing.
REFERENCES
1. Fukuyama J, Hayasaka S, Yamada K, Setogawa T. Causes of
subconjunctival hemorrhage. Ophthalmologica 1990;200(2):
63–67.
2. Pitts JF, Jardine AG, Murray SB, Barker NH. Spontaneous
subconjunctival haemorrhage: a sign of hypertension?
Br J Ophthalmol 1992;76(5):297–299.
3. Pearlman JA, Au Eong KG, Kuhn F, Pieramici DJ. Airbags and
eye injuries: epidemiology, spectrum of injury, and analysis
of risk factors. Surv Ophthalmol 2001;46(3):234–242.
4. Kenyon KR. Recurrent corneal erosion: pathogenesis and
therapy. Int Ophthalmol Clin 1979;19:169–195.
66
5. Brown NA, Byron AJ. Recurrent erosion of the cornea.
Br J Ophthalmol 1976;60:84–96.
6. Arbour JD, Brunette I, Boisjoly HM, Shi ZH, Dumas J, Guertin
C. Should we patch corneal erosions? Arch Ophthalmol
1997;115:313–317.
7. Kaiser PK. A comparison of pressure patching versus no
patching for corneal abrasions due to trauma or foreign body
removal. Corneal Abrasion Patching Study Group.
Ophthalmology 1995;102:1936–1942.
8. Rosenwasser GO. Complications of topical ocular anesthetics.
Int Ophthalmol Clin 1989;29(3):153–158.
9. Hamill MB. Corneal injury. In: Krachmer JH, Mannis MJ,
Holland EJ, eds. Cornea: Fundamentals of Cornea and
External Disease. Vol. 2. St. Louis: Mosby; 1997;1416–1419.
10. Ralph RA. Chemical injuries of the eye. In: Tasman W, Jaeger
EA, eds. Duane’s Clinical Ophthalmology. Vol. 4. Philadelphia:
Lippincott, Williams, and Wilkins; 1998:1–23.
11. Wagoner MD. Chemical injuries of the eye: current concepts
in pathophysiology and therapy. Surv Ophthalmology
1997;41(4):275–313.
12. Yu JS, Ralph RA, Rubenstein JB. Ocular burns. In: MacCumber
MW, ed. Management of Ocular Injuries and Emergencies.
Philadelphia: Lippincott-Raven; 1998:163–171.
13. Pfister DA, Pfister RR. Acid injuries of the eye. In: Krachmer JH,
Mannis MJ, Holland EJ, eds. Cornea: Fundamentals of Cornea
and External Disease. Vol. 2. St. Louis: Mosby; 1997:1437–1442.
14. Pfister RR, Pfister DA. Alkali-injuries of the eye. In: Krachmer
JH, Mannis MJ, Holland EJ, eds. Cornea: Fundamentals of
Cornea and External Disease. Vol. 2. St. Louis: Mosby;
1997:1443–1451.
15. Lubeck D, Greene JS. Corneal injuries. In: Mathews J, Zun LS,
eds. Emergency Medicine Clinics of North America:
Ophthalmologic Emergencies and Ocular Trauma.
Philadelphia: WB Saunders; 1988:82–86.
16. Roper-Hall MJ. Thermal and chemical burns. Trans
Ophthalmol Soc UK 1965;85:631–653.
17. Brodovsky SC, McCarty CA, Snibson G, et al. Management of
alkali burns: an 11-year retrospective review. Ophthalmology
2000;107(10):1829–1835.
18. Perry HD, Hodes LW, Seedor JA, Donnenfeld ED, McNamara
TF, Golub LM. Effect of doxycycline hyclate on corneal
epithelial wound healing in the rabbit alkali-burn model:
preliminary observations. Cornea 1993;12(5):379–382.

Closed globe injuries:
anterior chamber
James T. Banta, Colleen M. Cebulla, Carolyn D. Quinn
INTRODUCTION
Contusive injuries to the anterior chamber are
exceedingly common. Although most are minor
and self-limited, permanent vision loss can result
if appropriate measures to detect severe injuries
are not initiated. The focus of this chapter will
be to review the major traumatic injuries in-
volving the anterior chamber with a particular
emphasis on examination, stabilization, and
treatment.
EVALUATION
The assessment of an acute ocular injury begins
after other life-threatening injuries have been
appropriately ruled out. Once this has been
accomplished, a thorough history concerning the
mechanism of injury is of paramount impor-
tance. Most injuries are due to projectile objects
whether from assault, work, or play. The type of
object, the presence of sharp edges, and the
speed the object was traveling should be specifi-
cally recorded.
If a possible open globe injury is suspected, a
screening slit lamp examination should be per-
formed prior to further testing. A complete
ophthalmic examination is then performed if the
globe is intact. Visual acuity should be taken
with corrective spectacles if available. Pinhole
acuity may be used if spectacle correction is
unavailable. The use of a near card is sometimes
necessary in the emergency setting. Pupillary
examination is critical. Contusive ocular injuries
frequently lead to traumatic mydriasis or iris
sphincter tears which can lead to anisocoria
6
(with the larger pupil typically on the injured
side). The swinging flashlight test is used to rule
out a relative afferent pupillary defect. Intra-
ocular pressure following a contusive injury can
be elevated (due to mechanical blockage of the
trabecular meshwork by hyphema or inflam-
matory cells) or decreased (due to diminished
aqueous production associated with traumatic
iritis).
Slit lamp examination is utilized to carefully
ascertain the status of anterior chamber struc-
tures. The conjunctiva is examined for the
presence of hemorrhage, lacerations, or foreign
bodies. The cornea is inspected for lamellar lac-
erations, epithelial abrasions, or foreign bodies.
Increased magnification and a small, thin beam
are used to evaluate the anterior chamber for the
presence of cells and proteinaceous debris (flare).
Circulating red blood cells are indicative of a
microhyphema, while white blood cells are seen
with traumatic iritis. The iris is carefully
inspected at the pupillary margin for iris sphinc-
ter tears. Typically a focal irregularity of the
pupil is present. Transillumination of the iris
may reveal an iridodialysis or cyclodialysis. The
remainder of the slit lamp and dilated fundus
examination should be carried out as outlined in
Chapter 3.
PATHOPHYSIOLOGY
Contusive injuries of the anterior segment (and
anterior portion of the posterior segment) share
a common mechanistic pathway. Force from a
blunt object typically indents the cornea sud-
denly and rapidly leading to rapid equatorial
67
 Ocular trauma
Figure 6.1 Contusive injury of the globe leads to
deformation of the cornea and subsequent equatorial
expansion of the globe. Aqueous is simultaneously
forced into the periphery of the anterior chamber.
(Adapted with permission from Berke SJ. Post-traumatic
glaucoma. In: Yanoff M, Duker JS, eds. Ophthalmology,
2nd edn. Philadelphia: Mosby; 2004:1518–1521.)
expansion and forceful movement of aqueous
into the anterior chamber periphery (Figure
6.1). The classic description of the seven areas of
traumatic ocular tears is illustrated in Figure
6.2.
TRAUMATIC MYDRIASIS AND SPASM
OF ACCOMMODATION
Introduction
Traumatic mydriasis and spasm of accommoda-
tion are frequent complications of ocular trauma.1
Symptoms include eye pain, tearing, photo-
phobia, discomfort when reading, and ocular
fatigue.1,2 The pupil is characteristically mid-
dilated and poorly reactive to light with no rela-
tive afferent pupillary defect (Figure 6.3). 3
Pathophysiology
The force generated during contusive trauma
results in injury to the iris (both sphincter and
68
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
The diagnosis of traumatic mydriasis is primarily
based on slit lamp examination. If traumatic
mydriasis is the only lesion present, a large round
pupil will be identified, whereas if iris sphincter
tears are present there may be a ‘D’-shaped
margin, shallow indentations, or tears extending
the length of the iris.1 Multiple defects may be
present.
Patients with ciliary spasm typically complain
of dull, aching pain and photophobia. Cyclople-
gics paralyze the ciliary muscle, thereby prevent-
ing spasm and relieving pain. Treatment is
typically not needed outside the acute phase.
The prognosis of traumatic mydriasis and
accommodative paralysis is generally good. While
the problems with pupillary dilation and accom-
modation are often transient, a small but signifi-
cant percentage of patients will experience
lasting dilation and mild visual effects from
accommodative paralysis.1,4 In an analysis by
Tönjum, 14 of 35 eyes with traumatic mydriasis
and angle recession recovered a normal pupil size
by 4 months after injury.4 In another series, only
4 of 212 eyes with traumatic mydriasis were
permanently affected.5
Photophobia and blurred vision are frequently
encountered when traumatic mydriasis does not
resolve spontaneously and the pupil remains
 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

Figure 6.3 Traumatic mydriasis is seen in the right eye
following an industrial accident. A painted contact lens
was successfully used to limit debilitating glare induced
by the enlarged pupil.
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
attempt to diminish unwanted side-effects. If
unsuccessful, the concentration can be escalated
until symptoms diminish or side-effects become
prohibitive. Side-effects of pilocarpine include
induced myopia, brow ache, ciliary spasm,

69
 Ocular trauma
conjunctival injection, and reduced visual acuity
in dim illumination, particularly if lens opacities
are present. Thymoxamine, an alpha antagonist,
has shown some effectiveness in small clinical
trials, but is seldom used clinically. Tinted
contact lenses are an excellent option to improve
functionality and cosmesis. Hand-painted as
well as dyed lenses are commercially available
and assist in decreasing glare and photophobia.
Finally, surgical repair of the iris can be consid-
ered in conjunction with other procedures such
as cataract extraction.
TRAUMATIC IRITIS
Introduction
Traumatic iritis is one of the most frequent fi nd-
ings after contusive ocular trauma. Symptoms
are similar to other forms of iritis and include
pain, photophobia, and mildly decreased vision.
The intraocular pressure (IOP) is often lower in
the injured eye due to ciliary body dysfunction,
although elevated IOP can occur.6 The classic
slit lamp fi nding is anterior chamber cells and
flare. Traumatic iritis is often seen in conjunc-
tion with traumatic mydriasis and spasm of
accommodation.
Pathophysiology
Contusive ocular trauma causes an initial vaso-
spasm of the anterior uveal vessels, followed by
hyperpermeability. 3 This permeability allows a
delayed leakage of protein and fibrin into the
anterior chamber. A transient, scant release of
white blood cells typically occurs in this period.
Rarely, a more severe uveitis may develop, even
creating an endophthalmitis-like presentation.
Histopathologically, chronic inflammatory cells
are demonstrated infi ltrating the ciliary body.1
The ciliary body inflammation typically leads to
hypoproduction of aqueous fluid and subsequent
lowering of intraocular pressure.
70
Diagnosis and treatment
Photophobia, pain, and blurred vision are the
symptoms most frequently elicited. Although
symptoms can arise rapidly following severe
injuries, the presentation is often delayed 3–4
days following a mild contusive injury.
As mentioned above, the IOP can be quite
variable although relative hypotony compared to
the uninvolved eye is most frequently encoun-
tered. Diagnosis of traumatic iritis requires
visualization of anterior chamber cells and flare.
These fi ndings are best seen under high magni-
fication with a short, narrow slit beam placed
tangentially at maximum intensity. Prominent
perilimbal injection is often seen and is referred
to as a ciliary flush.
The treatment of choice for traumatic iritis is
cycloplegia (isoptohyoscine or atropine 1% two
to four times daily) alone or in combination with
a steroid drop (prednisolone acetate 1% four
times daily). Treatment is typically necessary for
only a short time (1–2 weeks), although a more
persistent and exuberant cellular reaction has
been described.6
IRIS SPHINCTER TEARS
AND IRIDODIALYSIS
Introduction
Iris sphincter tears and iridodialyses are com-
monly seen after contusive trauma to the eye.
Patients with iris sphincter tears or iridodialyses
may complain of changes to the shape of the
pupil, monocular diplopia (if the tear permits
light to travel to the retina outside the visual
axis), glare, decreased vision, and sensitivity to
light.
Pathophysiology
Iridodialysis is the shearing of the iris from the
ciliary body at the iris root. The iris is thinner
at this point, and more susceptible to injury.
 Closed globe injuries: anterior chamber

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 and treatment
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
2. debilitating glare11
3. expulsive iridodialysis (a rare condition in trau-
matized eyes with a history of ocular surgery)12
4. repair in conjunction with other planned
anterior segment surgery
5. cosmesis
6. subtotal iridodialysis associated with
8
glaucoma.
Several surgical techniques have been described
to treat iridodialysis. Removal of iris tissue may
be necessary if necrosis ensues, but repositioning
is always preferred if possible. Original surgical
techniques utilized a 10-0 polypropylene suture
on a 17 mm straight needle inserted 180 degrees
from the center of the iridodialysis and passed
through the damaged iris before being secured
to the sclera under a scleral flap. Popular variants
CASE EXAMPLES
Case report: iridodialysis (Figure 6.7)
A 16-year-old male reports glare, monocular diplopia
and decreased vision in the left eye 4 months after
suffering a paintball injury. He initially had a small
hyphema which was treated uneventfully. Initial
visual acuity was 20/40. Examination of the left eye
revealed a large nasal iridodialysis and an anterior
subcapsular cataract (A). The patient subsequently
underwent phacoemulsification (B) with intraocular
A B
72
of this technique (McCannel suture technique)
utilize a double-armed suture. Both arms of the
suture pass through the damaged iris several
millimeters apart and exit under a scleral flap
posterior to the limbus. The sutures are secured
under the flap creating a mattress suture.8,13,14
Closed chamber surgical techniques using
needles that hold a suture have also been used
successfully to treat iridodialysis without creat-
ing an incision in the anterior chamber.15–17 Iri-
dodialysis repair has been successfully combined
with other anterior chamber surgeries such as
trabeculectomy, pars plana vitrectomy, and cata-
ract surgery.18–20 Complications are uncommon,
but suture erosion has been described and is of
particular concern in children and young adults
because of softer sclera and a longer duration the
sutures will remain in place.10
lens implantation. Using a McCannel suture tech-
nique, the iris was reapproximated nasally and the
sutures were buried under a partial-thickness scleral
flap (C). Postoperatively, the patient recovered vision
to 20/20 with complete resolution of the monocular
diplopia and glare. Anatomically, the iris was reap-
proximated with minimal distortion of the pupil
(D).
Included
on DVD
 Closed globe injuries: anterior chamber

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

76

1. combination timolol/dorzolamide drops twice
daily
2. brimonidine drops twice daily
3. oral acetazolamide
4. prostaglandin analogue once daily.
Surgical intervention is sometimes necessary
when IOP is not controlled adequately with
medical therapy or if corneal blood staining
occurs. Prolonged elevated IOP can cause pro-
gressive optic nerve injury leading to decreased
vision and visual field defects. An ischemic
optic neuropathy can be induced by a severely
elevated IOP or even a moderately elevated
IOP in patients with sickle cell anemia. Corneal
blood staining can severely limit visual acuity
and can cause amblyopia in children. The timing
of surgical intervention depends greatly on the
extent and duration of IOP elevation and the
presence of corneal blood staining. Criteria
for surgical intervention developed by Read24
include:
1. microscopic corneal blood staining
2. total hyphema with intraocular pressures of
50 mmHg or more for 5 days (to prevent optic
nerve damage)
3. hyphema that is initially total and does not
resolve below 50% at 6 days with intraocular
pressures of 25 mmHg or more (to prevent
corneal blood staining)
4. hyphema that remains unresolved for 9 days
(to prevent peripheral anterior synechiae).
When sickling hemoglobinopathies are present,
criteria for surgical intervention are more
stringent:
1. repeated IOP measurements over 30 mmHg
2. mean IOP > 24 mmHg in the fi rst 24 hours
following injury.
These guidelines are tailored to the clinical situ-
ation and are not considered hard and fast rules.
Closed globe injuries: anterior chamber
Surgical techniques to lower intraocular pres-
sure following hyphema include anterior chamber
(AC) washout with or without trabeculec-
tomy. 35,36 It is vital to minimize the amount of
manipulation during surgery. AC washout uti-
lizes an entry and an exit paracentesis placed
180 degrees away from one another. As balanced
salt solution is gently irrigated into the eye, the
opposite paracentesis is gaped to allow gentle
egress of the blood clot. The goal of AC washout
is to debulk the organized hyphema present in
the anterior chamber, thereby removing a portion
of the mechanical blockage of the trabecular
meshwork that is partially responsible for ele-
vated IOP. Excessive manipulation and vigorous
irrigation should be avoided. The addition of a
trabeculectomy to AC washout allows continued
egress of blood and aqueous, both lowering IOP
and allowing more blood to exit the eye while
relieving pupillary block (if present). 37 The tra-
beculectomy often fails after a short period of
time, a result that is expected and in most cases
desirable.
The authors often utilize small-gauge biman-
ual vitrectomy through limbal corneal incisions.
The separation of irrigation and vacuum while
maintaining a relatively closed environment
allows for a gentle, controlled removal of the
hyphema. It is vital to maintain the least amount
of flow possible to remove the hyphema and
avoid excessive manipulation within the anterior
chamber. The crystalline lens, iris, and corneal
endothelium should be given a wide berth to
avoid iatrogenic injury. Whatever method is
used, the goal is only to debulk the organized
hyphema. Overzealous attempts to completely
clear the anterior chamber can cause rebleeding
or damage to intraocular structures.
77
Ocular trauma
CASE EXAMPLES
Case report: hyphema (Figure 6.10)
A 17-year-old male accidentally poked himself in the
right eye with the blunt end of a writing pen. He
noted immediate decreased vision and pain. He pre-
sented to the emergency room with a visual acuity
of light perception in the involved eye and an intra-
ocular pressure of 10. A 1.5 mm hyphema was noted
in the anterior chamber. The patient was started on
topical steroids and cycloplegia and instructed to
return the next day. The patient returned the follow-
ing day complaining of increased pain. A complete
hyphema was now present although intraocular
pressure remained normal. Over the course of a week,
although the hyphema began to contract into a
central clot (A), intraocular pressure continued to
increase despite aggressive medical therapy. Six days
after initial presentation, intraocular pressure was 51.
A B
78
The decision was made to proceed with removal of
the anterior chamber clot. Bimanual vitrectomy
instrumentation was introduced through two limbal
incisions and the clot was removed successfully (B).
The iris and lens were given a wide berth throughout
the procedure. The pressure decreased from 35 on
the first postoperative day to 14 on the third post-
operative day. The anterior chamber remained free
of blood. Once the clot had been removed, an iris
sphincter tear was now visible superiorly leading
to a typical D-shaped deformity of the pupil.
Importantly, it was apparent the anterior lens capsule
had been successfully avoided as retroillumination
revealed a clear lens (C). The patient recovered vision
of 20/25.

Case report: hyphema (cont’d)
All cases are not equally successful. Despite prompt
and appropriate care, poor outcomes are frequently
encountered, often related to concomitant injuries.
A 15-year-old male was punched in the right eye.
Initially he complained of pain, but his vision was
only mildly blurred. Four days following the injury,
he experienced sudden onset of severe pain and
decreased vision. Initial evaluation of the right eye
revealed a vision of light perception and an intraocu-
lar pressure of 50. Slit lamp examination revealed a
total hyphema (D). The patient was started on
aggressive medical treatment to control the intra-
ocular pressure. He initially received isosorbide and
later intravenous mannitol. Despite maximum
medical therapy, pressure remained in the 30s. A
decision was made to intervene surgically. An
anterior chamber washout (E) and trabeculectomy
D E
Included
on DVD
F G
Closed globe injuries: anterior chamber
(F) were performed. Although the anterior chamber
washout was initially successful, reaccumulation of
the anterior chamber blood was noted in the follow-
ing days. The intraocular pressure was better con-
trolled following surgery. The situation became more
complicated when a follow-up ultrasound revealed
a retinal detachment. Pars plana vitrectomy and
lensectomy were performed to repair a giant retinal
tear with an associated fibrotic retinal detachment.
Silicone oil tamponade was utilized. In the following
days, the hyphema reaccumulated once again and
pressures were again elevated, likely due to anterior
movement of silicone oil. Corneal blood staining was
soon evident (G). Despite slow clearing of the corneal
blood staining, vision never improved beyond light
perception.
79
 Ocular trauma
Complications and outcomes
As illustrated in the case reports, the visual
prognosis for patients with hyphema is quite
variable and depends on intraocular pressure,
rebleeding, the amount of blood at presentation,
and the presence of concomitant injury.
Rates of corneal blood staining vary depending
on the size of the initial hyphema and the extent
and duration of elevated intraocular pressures.
However, there have been multiple reports of
patients with normal IOP and a small hyphema
who develop visually significant corneal blood
staining.26,38 It is postulated that the combina-
tion of endothelial cell dysfunction and the toxic
effect of the blood breakdown products allows
the penetration of hemoglobin and hemoglobin
breakdown products into the posterior stroma. 39,40
Initially the deep stroma will have a yellowish
discoloration and pigment granules can be seen
in the posterior one third of the cornea. Close
examination of the posterior corneal is critical in
all patients with hyphemas. Corneal blood stain-
ing initially clears in the periphery of the cornea
and can take months to years to completely clear
centrally. 38 Corneal blood staining can have
potentially devastating results in children due to
deprivation amblyopia, and penetrating kerato-
plasty may be necessary to prevent severe
amblyopia.
The prevalence of sickle cell trait in the African-
American population is approximately 10%.41
Patients with sickle cell trait and sickle cell
disease are at risk for developing severe IOP
spikes, as sickled red blood cells in the anterior
chamber readily obstruct the trabecular mesh-
work. In all African-American patients a careful
history should be taken and a sickle cell prepara-
tion should be ordered, even if family history is
negative. In addition to the rapid IOP rises, sickle
cell patients are also at a higher risk for rebleed-
ing. In a published series of 99 children with
hyphema, nine patients (9%) had rebleeding, all
80
of whom were African-American and sickle cell
trait positive. The rate of rebleeding in Cauca-
sian and non-sickle cell trait African-American
children was 0%. Overall, nine of 14 patients
(64%) who tested positive for sickle cell trait had
rebleeding.41
Patients with sickling hemoglobinopathies are
more susceptible to vascular occlusive events at
lower pressures than normal individuals. Central
retinal artery occlusions in sickle cell patients
with pressures between 30 and 39 mmHg have
been reported.41,42 Dehydration can lead to
hyperviscosity and an increased risk of vascular
occlusion. For this reason, systemic hyperos-
motic agents and diuretics should be used with
great caution or avoided entirely. As described
above, carbonic anhydrase inhibitors should
always be avoided because they promote anterior
chamber sickling due to induced acidosis.
Other complications of hyphema include
peripheral anterior synechiae, optic atrophy (due
to contusion of the optic nerve, elevated intra-
ocular pressure, or vascular occlusion), accom-
modative impairment, cataract formation, and
angle recession.24,26 Visual acuity outcomes for
hyphema can be quite variable. Approximately
75% of patients will achieve a visual acuity of
20/50 or better.43 In a recent prospective study,
Rocha et al. reported a series of 35 children of
whom 75% achieved a visual acuity of 20/25
or better.44 Poor visual acuity outcomes were
due to retinal detachment, lens subluxation,
commotio retinae, and vitreous hemorrhage.
Although nearly half of these patients had ele-
vated IOP (>24 mmHg), all were controlled with
medical therapy.
ANGLE RECESSION
Introduction
Angle recession is an uncommon, yet underdiag-
nosed entity. Any severe contusive trauma,

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
can create a split in the ciliary body. The longi-
tudinal muscle of the ciliary body remains
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
and widening of the anterior chamber angle.
Small branches of the anterior ciliary artery are
often injured during this process, which explains
the frequent coexistence of hyphema and angle
recession.46
The development of glaucoma associated with
angle recession is not fully understood. Scarring
of the trabecular meshwork, loss of intertrabecu-
lar spaces, and scarring of Schlemm’s canal
results in decreased aqueous outflow and subse-
quent elevations in IOP.47–51 The greater the
portion of angle involved, the greater the subse-
quent risk of glaucoma. Glaucoma rarely devel-
ops if less than 180 degrees of angle is
involved.
Diagnosis and treatment
Gonioscopy is the mainstay of diagnosis in angle
recession. It is avoided during the acute phase of
Included
ocular injury if a hyphema is present. The angle
on DVD
appearance can be quite variable after a contu-
sive injury and it is best to compare the angles
of both eyes using a Zeiss or Goldman lens. Signs
of previous trauma including corneal scars,
Closed globe injuries: anterior chamber
Figure 6.11 Gonioscopic view of angle recession with a
broad yet irregular band of visible ciliary body. Note
the irregular, undulating contour of the iris root.
pigment deposition, tears in the iris sphincter,
iridodialysis, iridodonesis, phacodonesis, and
focal cataract formation are clues to prior signifi-
cant ocular injury.
Subtle changes include disruption of the iris
processes from their insertion into the scleral
spur and ciliary body leaving the ciliary body
more exposed.51 In more severe injuries, the
degree of angle recession may be larger and man-
ifest as a widened ciliary body band and a more
prominent scleral spur (Figure 6.11). Often it is
necessary to compare the width and color of the
ciliary body band to the fellow eye if the entire
angle is involved. It is important to assess the
extent of the angle recession. The extent of angle
involvement is directly correlated to the future
development of glaucoma.47
After establishing the extent of the angle
involved, it is critical to emphasize to the patient
the need for lifelong follow-up. Careful docu-
mentation of the IOP and optic nerve should be
completed. Initially, the IOP can be managed
medically. Miotics should be avoided because
they are ineffective and can rarely cause an ele-
vated IOP due to a decrease in uveoscleral
81
 Ocular trauma
outflow. All other classes of glaucoma medica-
tions may be effective. Laser trabeculoplasty is
usually ineffective in cases of traumatic glau-
coma.52,53 Ultimately, many patients with angle
recession glaucoma are inadequately controlled
and require surgical intervention.
Complications and outcomes
Approximately 6–8% of patients with angle
recession will ultimately develop glaucoma.47,51
It is possible that patients in this group also have
a predisposition to develop glaucoma, given that
50% of patients with traumatic glaucoma will
develop primary open angle glaucoma in their
fellow eye.54 If the IOP is not adequately con-
trolled, progressive optic neuropathy can occur.
Prior to the use of anitmetabolites such as 5-
fluorouracil and mitomycin-C, trabeculectomy
success rates were disappointing with rates as
low as 6–8% 5 years postoperatively.55 Manners
et al recently reported a series of 41 patients who
underwent trabeculectomy with mitomycin C
for traumatic glaucoma with an improved success
rate of 85% at 1 year and 66% at 3 years.56 Other
surgical options include the use of drainage
device implants. Ultimately the visual acuity
outcome depends on the presence of coexisting
ocular injuries and adequate IOP control.
CYCLODIALYSIS
Introduction
Traumatic cyclodialysis is an uncommon condi-
tion and can sometimes be difficult to diagnose.
A cyclodialysis cleft forms when a portion of the
ciliary body is disinserted from the sclera, allow-
ing free passage of aqueous into the suprachoroi-
dal space. Eye pain, tenderness, and decreased
vision are common presenting symptoms. Severe
hypotony is the hallmark of the condition and
can lead to corneal failure and eventually phthi-
sis bulbi if left untreated.
82
Pathophysiology
Rapid equatorial expansion of the eye during
contusive injury can cause disinsertion of the
ciliary body from the scleral spur. Historically,
communication between the anterior chamber
and suprachoroidal space following cyclodialysis
was confi rmed surgically when fluorescein was
injected into the anterior chamber, and fluores-
cein staining of the fluid drained externally from
the suprachoroidal space was noted. The free
passage of aqueous into the suprachoroidal
space leads to hypotony as the potential space of
the suprachoroidal space has a much greater
volume than the anterior chamber. Ciliochoroi-
dal detachments often form and lead to further
dysfunction of the ciliary body, diminished
aqueous production, and further hypotony.
These two factors in concert with inflammation
from the inciting trauma often lead to profound
hypotony,57,58 the hallmark of a cyclodialysis
cleft.
Diagnosis and treatment
The diagnosis of cyclodialysis depends primarily
on tonometry, slit lamp examination, gonios-
copy, and dilated fundus exam.59 Blurred vision
with a hyperopic shift may be present due to
anterior displacement of the lens–iris diaphragm
and overall shortening of the eye. Hypotony,
often profound, is the classic fi nding. Anterior
chamber signs include corneal edema, shallow-
ing of the anterior chamber, mydriasis, and a
peaked pupil near the cyclodialysis site. If hypo-
tony is persistent, optic disc edema, retinal vessel
tortuosity, and retinal and choroidal folds are
often seen.59,60 Many cyclodialyses can be visual-
ized with gonioscopy and appear as a gap between
the sclera and the ciliary body. Ultrasound bio-
microscopy is a newer technique which offers
promise in diagnosing occult cyclodialyses, espe-
cially when the view is obscured by hemorrhage
or corneal edema.61,62 Cyclodialysis clefts become

increasingly difficult to visualize as time passes,
as peripheral anterior synechiae form and obscure
the anterior chamber angle.50 Ultrasound can
facilitate diagnosis and localization in these more
difficult cases.
Many treatments have been developed for
cyclodialysis.59 Observation or medical therapy
with cycloplegics is initially attempted, but
further treatment is often required to defi ni-
tively close the cleft. Atropine is used initially to
maintain anatomic proximity of the ciliary body
and scleral spur, thereby encouraging closure of
the cleft. Corticosteroids are thought to delay
closure of cyclodialysis clefts, and are generally
not recommended unless required for concomi-
tant injuries.
The classic treatment of cyclodialysis for many
years was pupillary dilation in conjunction with
diathermy applied to the cyclodialysis cleft, fol-
lowed by drainage of suprachoroidal effusions
through incisions in the sclera.63 Flattening the
communication with the suprachoroidal space
would often lead to reattachment of the ciliary
body and restoration of function. In an impor-
tant treatment advance, Joondeph was the fi rst
to use argon laser to successfully treat cyclodialy-
sis.60 Argon laser applied to the cyclodialysis
cleft has now become the fi rst line of therapy if
medical management does not achieve success in
the fi rst 4–6 weeks.58 Laser is applied to the
ciliary body and scleral sides of the cleft. Recom-
mended settings are:
1. duration of 0.1 second
2. 50–100 micron spot size
3. 500–1500 mW power
4. approximately 100 applications.
Atropine is continued after treatment. If the
initial treatment is unsuccessful, repeat treat-
ments often will close the cyclodialysis cleft. If
the anterior chamber is relatively flat, obscuring
the view of cyclodialysis clefts, viscoelastic injec-
tion into the anterior chamber is helpful in deep-
Closed globe injuries: anterior chamber
ening the anterior chamber and exposing the
cleft for laser therapy.59
Although many cyclodialysis clefts respond to
laser treatment, invasive surgical treatments are
recommended if argon laser therapy fails.59,64–67
The classic treatment of diathermy described
by Maumenee and Stark remains a reasonable
second-line therapy.63 Direct cyclopexy has been
more recently advocated. In this technique, the
ciliary body is sutured directly to the sclera in
the area of the cleft by way of a partial- or full-
thickness scleral flap. Indirect cyclopexy has also
been reported using a McCannel suture similar
to repair of iridodialysis, and this technique may
be effective for smaller clefts. Anterior scleral
buckle may be effective, especially if the cleft
area is very large.
Other generally less invasive techniques have
also been reported to be successful in treat-
ing cyclodialysis including cryotherapy, YAG
laser cyclophotocoagulation, and argon laser
endophotocoagulation.68–72
Complications and outcomes
Successful treatment of cyclodialysis results in
closure of the cleft and an acute increase in IOP
and eye pain.58,59 Patients should be instructed
to contact their physician if they experience
severe eye pain. The rise in IOP is typically
delayed by 1–2 weeks when indirect treatments
are used (e.g. argon laser) but can be very rapid
following direct cyclopexy. This ocular hyper-
tensive period is typically transient and thought
to be due to delayed opening of aqueous drainage
channels that collapse during prolonged hypoto-
nous periods. Topical and oral aqueous suppres-
sants are used to manage these transient episodes.
Pilocarpine can facilitate reopening of the cleft
and should be avoided.
The prognosis of cyclodialysis with treatment
is surprisingly good.59 Although delayed closure
may reduce visual acuity, patients have been
83
 Ocular trauma
reported to improve even after long periods of
hypotony, including one case of visual improve-
ment from 20/200 to 20/30 after 7 years of
CASE EXAMPLES
Case report: cyclodialysis cleft (Figure 6.12)
A 26-year-old male was hammering a nail when the
nail became dislodged and struck him in the left eye.
He was placed on atropine and prednisolone acetate
by an ophthalmologist. A month later, he presented
to our emergency clinic with complaints of declining
vision in the left eye. Initial visual acuity was 20/200
in the left eye with an intraocular pressure of 6. Slit
lamp examination revealed a subtle abnormality in
the contour of the temporal pupillary margin and a
suspicious area in the temporal anterior chamber
angle (A). Gonioscopy revealed a temporal cyclo-
dialysis cleft (B). Dilated fundus exam revealed
optic nerve edema, retinal vascular tortuosity, and
macular edema with retinal folds (C). A diagnosis of
hypotony maculopathy secondary to the cyclodialy-
sis cleft was made. Argon laser photocoagulation
was applied to the bed of the cleft and prednisolone
acetate was tapered quickly. Atropine was continued
four times daily. Four days later, the situation was
unchanged and further argon laser was applied (D).
A B
84
hypotony.72 Concomitant traumatic injuries of
the posterior segment are often responsible for
poor visual outcomes when they occur.
One week later, the patient presented to the emer-
gency clinic again with complaints of pain in the left
eye. Vision had improved to 20/70 and intraocular
pressure was 34. Timolol and dorzolamide were
applied and the intraocular pressure was quickly
normalized. Vision continued to slowly improve. At
the final follow-up 18 days following the second
round of argon laser photocoagulation, visual acuity
was 20/20 and intraocular pressure was normal.
Dilated fundus exam revealed vast improvement in
the optic nerve edema and vascular tortuosity,
although some retinal folds persisted (E). Before and
after OCT evaluation shows marked improvement in
macular edema, subretinal fluid, and chorioretinal
architecture (F). (From Goldman D, Moore J, Greulich
K, Flynn HW Jr. Cyclodialysis and hypotony macu-
lopathy. Ophthalmic Surgery, Lasers & Imaging.
37:438–9, 2006 with permission from SLACK
Incorporated.)
 Closed globe injuries: anterior chamber

Case report: cyclodialysis cleft (cont’d)

C D

E F

SUMMARY 4. Large traumatic iridodialyses may lead to

1. Anterior chamber injuries are some of the
most frequently encountered sequelae of con-
tusive ocular injury.
2. Traumatic mydriasis is typically self-limited,
but occasionally can lead to chronic symptom-
atic glare and blurred vision.
3. Traumatic iritis is treated successfully with
cycloplegics. Steroid drops may be necessary
for significant inflammation.
chronic glare and diplopia and often require
surgical repair.
5. Traumatic hyphema is treated on an outpa-
tient basis unless follow-up or the application
of medications can not be assured (e.g. young
children).
6. Sickle cell screening should be performed on
all African-American and African-Caribbean
patients with hyphema regardless of family
history.

85
 Ocular trauma
7. Steroids, aminocaproic acid, and cycloplegics
are accepted medical treatments for hyphema.
Anterior chamber washout with or without a
trabeculectomy is necessary when medical
treatments fail to maintain an appropriate
intraocular pressure or corneal blood staining
occurs.
8. The mainstays for visualization of cyclodialy-
sis clefts are gonioscopy and, more recently,
ultrasound biomicroscopy.
9. Cyclodialysis resolution can be obtained with
cycloplegia, argon laser, or surgical repair and
success is heralded by a severe yet transient
elevation in intraocular pressure.
REFERENCES
1. Kilgore GL. Changes in the ciliary body after contusion bulbi
in which only the anterior segment of the eye is affected.
Am J Ophthal 1942;25:1095–1099.
2. Sharma A, Votruba M. Thymoxamine in the treatment of
traumatic mydriasis. Br J Ophthal 1993;77:681.
3. Duke-Elder, S. Textbook of Ophthalmology. Vol. VI, Injuries.
St. Louis, MO: C.V. Mosby; 1954:5774–5799.
4. Tönjum AM. Gonioscopy in traumatic hyphema. Acta
Ophthalmol 1966;44:650–664.
5. Canavan YM, Archer DB. Anterior segment consequences of
blunt ocular injury. Br J Ophthalmol 1982;66:549–555.
6. Eagling EM. Ocular damage after blunt trauma to the eye.
Br J Ophthalmol 1974;58:126–140.
7. Kumar S, Miller D, Atebara N, Blance E. A quantitative animal
model of traumatic iridodialysis. Acta Ophthalmol 1990;68:
591–596.
8. Cauchi P, Chen HC, Holden R. Primary surgical management
in a case of subtotal iridodialysis. Eye 1999;13:791.
9. Howard GM, Hutchinson BT, Frederick AR. Hyphema resulting
from blunt trauma; gonioscopic, tonographic, and
ophthalmoscopic observations following resolution of the
hemorrhage. Tr Am Acad Ophth & Otol 1965;69:294–306.
10. Abbott RL, Spencer WH. Epithelialization of the anterior
chamber after transcorneal (McCannel) suture. Arch
Ophthalmol 1978;96:482–484.
11. Kaufman SC, Insler MS. Surgical repair of a traumatic
iridodialysis. Ophthal Surg Lasers 1996;27:963–966.
12. Navon SE. Expulsive iridodialysis: an isolated injury after
phacoemulsification. J Cataract Refract Surg 1997;23:805–807.
86
13. Wachler BB, Krueger RR. Double-armed McCannell suture
for repair of traumatic iridodialysis. Am J Ophthalmol
1996;122:109–110.
14. Oshika T, Amano S, Kato S. Severe iridodialysis from
phacoemulsification tip suction. J Cataract Refractive Surg
1999;25:873–875.
15. Zeiter JH, Shin DH, Shi DX. A closed chamber technique for
repair of iridodialysis. Ophthal Surg 1993;24:476–480.
16. Bardak Y, Ozerturk Y, Durmus M, Mensiz E, Aytuluner E. Closed
chamber iridodialysis repair using a needle with a distal hole.
J Cataract Refract Surg 2000;26:173–176.
17. Erakgun T, Kskaloglu M, Kayikcioglu O. A simple closed
chamber technique for repair of traumatic iridodialysis in
phakic eyes. Ophthal Surg Lasers 2001;31:83–85.
18. Chang S, Coll GE. Surgical techniques for repositioning a
dislocated intraocular lens, repair of iridodialysis, and
secondary intraocular lens implantation using innovative
25-gauge forceps. Am J Ophthal 1995;119:165–174.
19. Lam DSC, Chua JKH, Kwok AKH, et al. Combined surgery for
severe eye trauma with extensive iridodialysis, posterior lens
dislocation, and intractable glaucoma. J Cataract Refract Surg
1999;25:285–288.
20. McBratney RT. Surgical technique for repositioning a
dislocated intraocular lens, repair of iridodialysis, and
secondary intraocular lens implantation using innovative
25-gauge forceps. Comment. Am J Ophthalmol 1995;120:
126.
21. Agapitos PJ, Noel LP, Clarke WN. Traumatic hyphema in
children. Ophthalmology 1987;94:1238–1241.
22. Wilson FM. Traumatic hyphema: pathogenesis and
management. Ophthalmology 1980;87:910–919.
23. Walton W, Von Hagen S, Grigorian R, Zarbin M. Management
of traumatic hyphema. Sur Ophthalmol 2002;47(4):297–334.
24. Read J. Traumatic hyphema: surgical vs medical
management. Ann Ophthalmol 1975;7:659–662.
25. Clever VG: Home care of hyphemas. Ann Ophthalmol
1982;14:25–27.
26. Read J, Goldberg MF. Comparison of medical treatment for
traumatic hyphema. Trans Am Acad Ophtlamolol Otolaryngol
1974;79:799–815.
27. Shiuey Y, Lucarelli MJ. Traumatic hyphema: outcomes of
outpatient management. Ophthalmology
1998;105(5):851–855.
28. Ng CS, Strong NP, Rosenthal AR. Factors related to the
incidence of secondary hemorrhage in 462 patients with
traumatic hyphema. Eye 1992;6:308–312.
29. Faber MD, Fiscella R, Goldberg MF. Amniocaproic acid versus
prednisone for the treatment of traumatic hyphema: a
randomized clinical trial. Ophthalmology 1991;98:279–286.

30. Ramono PE. Systemic prednisolone prevents rebleeding in
traumatic hyphema. Ophthalmology 2000;197:812–814.
31. Rahmani B, Jahadi HR. Comparison of tranexamic acid and
prednisolone in the treatment of traumatic hyphema: a
randomized clinical trial. Ophthalmology 1999;106:375–379.
32. Kutner B, Fourman S, Brein K, et al. Aminocaproic acid
reduces the risk of secondary hemorrhage in patients
with traumatic hyphema. Arch Ophthalmol 1987;105(2):
206–208.
33. Crouch Jr. ER, Williams PB, Gray K, Crouch ER, Chames M.
Topical amniocaproic acid in the treatment of traumatic
hyphema. Arch Ophthalmol 1997;115(9):1106–1112.
34. Pieramici DJ, Goldberg MF, Melia M, et al. A phase III,
multicenter, randomized placebo-controlled clinical trial of
topical aminocaproic acid (Caprogel) in the management
of traumatic hyphema. Ophthalmology 2003;110(11):
2106–2112.
35. Graul TA, Ruttum MS, Lloyd MA, Radius RL, Hyndiuk RA.
Trabeculectomy for traumatic hyphema with increased
intraocular pressure. Am J Ophthalmol 1994;117(2):155–159.
36. Belcher CD, Brown SV, Simmons RJ. Anterior chamber
washout for traumatic hyphema. Ophthalmic Surg
1985;16(8):475–479.
37. Parrish RK, Baradino V Jr. Iridectomy in the surgical
management of eight ball hyphema. Arch Ophthalmol
1982;100:435–437.
38. Brodrick JD. Corneal blood staining after hyphaema. Br J
Ophthalmol 1972;56:589–593.
39. Gottsch JD, Graham CR Jr, Hairston RJ, et al. Protoporphyrin
IX photosensitization of corneal endothelium. Arch
Ophthalmol 1989;107:497–500.
40. Gottsch JD, Messmer EP, McNair DS, Font RL. Corneal
blood staining: an animal model. Ophthalmology
1986;93:797–802.
41. Nasrullah A, Kerr N. Sickle cell trait as a risk factor for
secondary hemorrhage in children with traumatic hyphema.
Am J Ophthalmol 1997;123:783–790.
42. Crouch ER Jr, Frenkel M. Aminocaproic acid in the
treatment of traumatic hyphema. Am J Ophthalmol 1976;
81:355–360.
43. Edwards WC, Layden WF. Traumatic hyphema. Am J
Ophthalmol 1973;75:110–113.
44. Rocha KM, Martins EN, Melo LA Jr, Bueno de Moraes NS.
Outpatient management of traumatic hyphema in children:
prospective evaluation. J AAPOS 2004;8:357–361.
45. Wolff SM, Zimmerman LE. Chronic secondary glaucoma:
association with retrodisplacement of iris root and deepening
of the anterior chamber angle secondary to contusion. Am J
Ophthalmol 1962;84:547–563.
Closed globe injuries: anterior chamber
46. Spaeth GL. Traumatic hyphema, angle recession,
dexamethasone hypertension, and glaucoma. Arch
Ophthalmol 1967;78:714–721.
47. Blanton FM. Anterior chamber angle recession and secondary
glaucoma: a study of the after effects of traumatic hyphemas.
Arch Ophthalmol 1964;72:39–44.
48. Tonjum AM. Intraocular pressure and facility of outflow
late after ocular contusion. Acta Ophthalmol 1968;46:886–
908.
49. Wolff SM, Zimmermann LE. Chronic secondary glaucoma
associated with retrodisplacement of the iris root and
deepening of anterior chamber angle secondary to
contusion. Am J Ophthalmol 1962;54:547–563.
50. Herschler J. Trabecular damage due to blunt anterior
segment injury and its relationship to traumatic glaucoma.
Trans Am Acad Ophthalmol Otolaryngol 1977;83:239.
51. Kaufman J, Tolpin D. Glaucoma after traumatic angle
recession. Am J Ophthalmol 1974;78:648–654.
52. Thomas JV, Simmons RJ, Belcher CD III. Argon laser
trabeculoplasty in the presurgical glaucoma patient.
Ophthalmology 1982;89:187–191.
53. Robin AL, Pollack IP. Argon laser trabeculoplasty in secondary
form of open angle glaucoma. Arch Ophthalmol
1983;101:382–384.
54. Tesluk GC, Spaeth GL. The occurrence of primary open
angle glaucoma in the fellow eye of patients with unilateral
angle-cleavage glaucoma. Ophthalmology 1985;92(7):
904–911.
55. Mermound A, Salmon JF, Straker C, et al. Post-traumatic angle
recession glaucoma: a risk factor for bleb failure after
trabeculectomy. Br J Ophthalmol 1993;77:631–634.
56. Manners T, Salmon, JF, Barron A, Willies, Murray AN.
Trabeculectomy with mitomycin C in the treatment of post-
traumatic angle recession glaucoma. Br J Ophthalmol
2001;85:159–163.
57. Chandler PA, Maumenee AE. A major cause of hypotony.
Am J Ophthalmol 1961;52:609–618.
58. Aminlari A, Callahan CE. Medical, laser, and surgical
management of inadvertent cyclodialysis cleft with hypotony.
Arch Ophthalmol 2004;122:399–403.
59. Ormerod LD, Baerveldt G, Sunalp MA, Riekhof FT.
Management of the hypotonous cyclodialysis cleft.
Ophthalmology 1991;98:1384–1393.
60. Joondeph HC. Management of postoperative and
post-traumatic cyclodialysis clefts with argon laser
photocoagulation. Ophthalmic Surg 1980;11:186–188.
61. Berinstein DM, Gentile RC, Sidoti PA, et al. Ultrasound
biomicroscopy in anterior ocular trauma. Ophthalmic Surg
Lasers 1997;28:201–207.
87
 Ocular trauma
62. Özdal MPC, Mansour M, Deschenes J. Ultrasound
biomicroscopic evaluation of the traumatized eyes.
Eye 2003;17:467–472.
63. Maumenee AE, Stark WJ. Management of persistent hypotony
after planned or inadvertent cyclodialysis. Am J Ophthalmol
1971;71:320–327.
64. Küchle M, Naumann GO. Direct cryopexy for traumatic
cyclodialysis with persisting hypotony: report in 29
consecutive patients. Ophthalmology 1995;102:322–333.
65. Tate GW, Lynn JR. A new technique for the surgical repair of
cyclodialysis induced hypotony. Ann Ophthalmol 1978;10:
1261–1266.
66. Vannas M, Bjorkenheim B. On hypotony following
cyclodialysis and its treatment. Acta Ophthalmol
1952;30:63–64.
67. Viikari K, Tuovinen E. On hypotony following cyclodialysis
surgery. Acta Ophthalmol 1957;35:543–549.
88
68. Krohn J. Cryotherapy in the treatment of cyclodialysis
cleft induced hypotony. Acta Ophthalmol Scand
1997;75:96–98.
69. Brooks AMV, Troski M, Gillies WE. Noninvasive closure of a
persistent cyclodialysis cleft. Ophthalmology
1996;103:1943–1945.
70. Alward WLM, Hodapp EA, Parel JM, Anderson DR. Argon laser
endophotocoagulator closure of cyclodialysis clefts. Am J
Ophthalmol 1988;106:748–749.
71. Caronia RM, Sturm RT, Marmor MA, Berke SJ. Treatment of a
cyclodialysis cleft by means of ophthalmic laser
microendoscope endophotocoagulation. Am J Ophthalmol
1999;128:760–761.
72. Delgado MF, Daniels S, Pascal S, Dickens CJ. Hypotony
maculopathy: improvement of visual acuity after 7 years.
2001;32:931–933.

Closed globe injuries: lens
David A. Goldman, Jennifer I. Hui
INTRODUCTION
Lens injuries have been reported to occur in 7–
50% of eyes sustaining significant trauma.1–3
Patients with traumatic lens injuries may present
to the ophthalmologist immediately after sus-
taining an injury or at a much later time. Com-
plaints include decreased vision, fluctuating
vision, monocular diplopia, glare, or pain. In this
chapter we will discuss the history, evaluation,
and management strategies associated with
traumatic lens injuries and potential long-term
sequelae.
EVALUATION
History is invaluable when approaching trau-
matic lens injuries. The examiner must deter-
mine the time and mechanism of injury as well
as the timing, quality, and nature of the symp-
toms. In particular, the mechanism of injury will
help guide the examination and raise or lower
the suspicion of a possible eyewall violation or
intraocular foreign body. It is not uncommon for
patients with traumatic cataracts to present with
a remote history of trauma or sometimes a nega-
tive history altogether. Past ocular history, such
as previous surgery, is also an essential part of
the evaluation.
A thorough examination of the eye, as dis-
cussed in Chapter 3, is mandatory following any
ocular trauma. Lens injury frequently coexists
with other significant ocular injuries. A screen-
ing slit lamp examination is performed before
eye drops are instilled or intraocular pressure is
taken in order to determine the integrity of the
7
eyewall. Once this is complete, a careful system-
atic examination of the eye is performed.
Evaluation of the crystalline lens is an integral
part of the examination in a traumatized eye.
The position of the lens is fi rst determined. The
normal crystalline lens is held in place by the
lens zonules (Figure 7.1). Partial dehiscence of Included
on DVD
the lens zonules will lead to subluxation (Figure
7.2). Subluxation implies the crystalline lens is
still held in place by the remaining lens zonules
but is no longer centered in the pupillary space.
The elasticity of the remaining lens zonules pulls
the lens away from the site of zonular dehis-
cence. Often this is detected by visualizing the
curvilinear lens equator when the pupil is dilated.
Complete zonular dehiscence leads to lens dis-
location (Figure 7.3). A dislocated lens most
frequently falls into the vitreous cavity, but
occasionally can prolapse forward into the ante-
rior chamber. While a subluxated lens may be
asymptomatic if minimally decentered, com-
plete dislocation of the lens into the vitreous
cavity always leads to immediately decreased
vision, as the eye is functionally aphakic. Contu-
sive ocular injury can also cause diffuse damage
of the lens zonules leading to instability of the
lens and phacodonesis. Phacodonesis may range
from minimal shimmer of the crystalline lens to
frank, profound movement of the lens–iris dia-
phragm. To test for phacodonesis, the patient is
asked to look away from the slit lamp beam and
then rapidly return gaze to the light. Gently
pounding the slit lamp table with a closed fist
while the patient looks straight ahead can some-
times produce similar results. Any movement of
the lens is attributable to zonular weakness and
89
 Ocular trauma
Visual axis Intact zonules
Crystalline lens
Figure 7.1 Diagrammatic representation of the normal
anatomic position of the crystalline lens supported 360
degrees by the lens zonules (iris not pictured).
should be documented at the time of initial
examination. Other signs that are indicative of
zonular weakness and often coexist with all
three of these conditions include iridodonesis,
asymmetric anterior chamber depth (the affected
side typically has the deeper chamber), an eccen-
tric pupil, or the presence of vitreous at the
pupillary margin or within the anterior chamber
(Figure 7.4).
If a corneal or anterior scleral laceration is
present, the examiner must carefully look for iris
transillumination defects, a disruption in the
anterior capsule or the presence of an intralen-
ticular foreign body. With an anterior laceration
and a violated lens capsule, the patient is assumed
to have an intraocular foreign body until proven
otherwise. If ultrasound fails to reveal a foreign
90
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,
corneal disease, or anterior segment disruption,
an imaging modality may be pursued. Options
include B-scan ultrasound, ultrasound biomicro-
scopy, CT, or MRI. CT and MRI may provide
important information about the lens and the
orbit, but are seldom indicated solely for locating
the lens. Ultrasound is more efficient and quickly
obtained and may be performed in an office
setting. When the view through the anterior
segment is clear and the lens is not visualized,
one must consider complete dislocation of the
lens into the vitreous cavity or through a site of
scleral rupture.1
DIAGNOSIS AND TREATMENT
General considerations
While initial trauma to the lens may appear insig-
nificant, delayed sequelae may present days to
months after the initial incident. These sequelae
are discussed below and are arranged in order of
when they would most likely present after the
 Closed globe injuries: lens

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-
location) to delayed by months or years (phaco-
lytic glaucoma). The specific treatment modalities
for each injury type are described in detail.
Lens subluxation and dislocation
(immediate to delayed)
Lens subluxation or dislocation, found alone or
in conjunction with other ocular injuries, is most
frequently caused by trauma.4 Lenticular sublux-
ation is not always evident with the traditional
slit lamp examination. For example, an inferior
zonular disruption may not be evident unless the
patient is in a supine position. Thus, a lens with
zonular weakness can change its position depend-
ing on the posture of the patient.5 If zonular
disruption is incomplete, the lens is typically
drawn away from the site of the zonular rupture
by the intact zonules. The anterior chamber
is often asymmetrically deep in this setting.6
B-scan ultrasound or ultrasound biomicroscopy
may aid in localization of the lens in eyes with
a suboptimal view of the anterior chamber.7,8
If the lens cannot be visualized, extraocular
displacement of the lens is also a consideration,
especially in patients with a history of large-
incision surgery (e.g. extracapsular cataract
extraction, penetrating keratoplasty). The lens
may have extruded through a previous surgical
wound or another site of structural disruption.
Scleral ruptures are not always visible and an
extruded crystalline lens may be found in a sub-
conjunctival location. 9 Scleral ruptures most fre-
quently occur between the limbus and the spiral
of Tillaux in the superonasal and superotempo-
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
secondary myopic lens changes.11 Monocular
diplopia is induced if the lens margin splits the
visual axis.
Rapid, severe vision loss results from posterior
dislocation of the lens as the eye becomes func-
tionally aphakic. Visual acuity can often be
improved with spectacles or a contact lens. A
contact lens may provide the most noteworthy
relief of symptoms as it reduces the amount of
induced anisometropia that occurs with mono-
cular aphakic spectacle correction. Symptoms
may also be minimized with miotics to prevent
pupillary dilation. Medical management of sub-
luxated or dislocated lenses is often preferable to
surgical options. Extraction of a subluxated cata-
ract is fraught with difficulties depending on
the degree of subluxation. Severely subluxated
lenses with vitreous prolapse are often referred to
vitreoretinal specialists for pars plana vitrectomy
and lensectomy. With milder degrees of subluxa-
tion, the use of capsular hooks and/or capsular
tension rings can stabilize the lens so that routine
phacoemulsification with posterior chamber in-
traocular lens implantation may be performed.
Intracapsular cataract surgery with anterior cham-
ber intraocular lens implantation is advocated by
some for severely subluxated cataracts without
vitreous prolapse. Surgeon experience will dictate
the appropriate removal strategy.
Traumatic lens dislocation into the anterior
chamber causes a severe loss of vision. Pupillary
Closed globe injuries: lens
Figure 7.5 Traumatic anterior lens dislocation with
diffuse contact between the corneal endothelium and
the crystalline lens.
block is often induced given the limited space in
the anterior chamber (Figure 7.5). Initial treat-
ment with anti-inflammatories and glaucoma
medications is initiated in preparation for defi ni-
tive surgery. Corneal–lenticular touch imparts a
significant risk of endothelial dysfunction and
subsequent corneal decompensation. Dilation is
not recommended as the lens may dislocate into
the vitreous and require a vitrectomy for removal.
Since most injuries occur in young patients, the
crystalline lens is often not cataractous and can
be readily aspirated once the capsular bag is
opened. If the lens is cataractous, phacoemulsi-
fication can be attempted. The cornea must be
relatively clear and the anterior chamber of
sufficient depth to ensure safe removal. In both
instances, viscoelastic is used to push the ante-
rior vitreous back to prevent inadvertent vitreous
traction. If vitreous presents, an anterior vitrec-
tomy is performed following cataract removal.
An anterior chamber or sutured posterior
chamber intraocular lens may be implanted at
the time of cataract extraction if the inflamma-
tion is sufficiently treated. If severe inflamma-
tion is present, the eye is often left aphakic.
Secondary intraocular lens implant can be per-
formed when the inflammation subsides. If the
anterior chamber is not sufficiently deep, the
93
 Ocular trauma
cataract is dense, small incision cataract surgery
is not possible, or significant vitreous prolapse is
present preoperatively, intracapsular extraction
or pars plana vitrectomy and lensectomy is
indicated.
The crystalline lens is more frequently dislo-
cated posteriorly into the vitreous cavity. Patients
have significant visual symptoms secondary to
functional aphakia. The status of the lens capsule
plays a vital role in determining appropriate treat-
ment. If the capsule is intact, the lens may remain
in the vitreous cavity without inciting inflamma-
tion. A violated capsule frequently leads to a
variable inflammatory response requiring sur-
gical lens removal after an initial course of anti-
inflammatories. A vitreoretinal surgeon provides
defi nitive surgical care. Most lenses are removed
by phacofragmentation through the pars plana
after a vitrectomy has been performed. If the lens
is too dense for phacofragmentation within the
vitreous, it may be brought into the anterior
chamber and removed through a limbal wound.6
Phacoanaphylactic uveitis (hours to years)
Phacoanaphylactic uveitis is a rare, aggressive
immune response mounted against exposed lens
proteins following traumatic lens capsule disrup-
tion. It is frequently associated with chemosis,
conjunctival injection, anterior chamber cell and
flare, large and multiple keratic precipitates, and
in severe cases, hypopyon. Rarely, the fellow eye
may develop similar inflammation. Typically, the
intraocular pressure is low; however, elevations
can also occur (see Lens-induced glaucoma,
below). Elevated intraocular pressure may be
reduced with topical beta-blockers, carbonic
anhydrase inhibitors, alpha-adrenergic blockers
or prostaglandin analogues. Intraocular inflam-
mation may be alleviated with steroids, either
topically, via sub-Tenon’s injection, or orally.
Removal of the lens, however, is the defi nitive
required treatment. Surgery is often deferred for
94
several days so the surgery can be performed in
a noninflamed and normotensive eye. Routine
phacoemulsification with posterior chamber
intraocular lens implantation can often be per-
formed depending on the mechanism of injury
and the amount of capsular disruption.
Traumatic cataract (days to years)
Cataracts may arise from contusive eye trauma
immediately after injury or many years later.
They are reported to occur in 11% of eyes with
closed globe injuries.2 The concept of ‘coup’ and
‘contrecoup’ forces was fi rst described by Wolter12
and Weidenthal and Schepens.13 These forces,
in addition to equatorial expansion of the globe,
are the postulated mechanisms of injury. ‘Coup’
refers to direct forces while ‘contrecoup’ refers
to injury occurring as a result of transmitted
shock waves through the lens. Equatorial expan-
sion of the globe occurs when it is shortened in
the anteroposterior direction at the time of
impact. Such expansion may result in lens cap-
sular rupture, zonular dehiscence, or both.14
Cataracts can form following disruption of the
lens capsule. A capsular defect allows aqueous
humor to enter the lens, leading to increasing
opacity until the flow of aqueous ebbs.15 The
natural history of lens capsule violation is unclear.
The anterior capsule has a high capacity for
healing because of the regenerative properties of
the subcapsular epithelium and is less suscepti-
ble to rupture given its greater thickness. If the
capsular defect is <2 mm, the epithelium rapidly
restores continuity. Defects larger than 3 mm
frequently lead to lenticular opacity. Healing of
the capsule limits passage of free ions and fluid
that may lead to cataract formation. The anterior
capsule may also spontaneously reopen, causing
severe inflammation and secondary glaucoma
days to months following injury.
Most traumatic cataracts are not associated
with capsular disruption. An ocular contusion

Figure 7.6 Classic petalloid anterior subcapsular
cataract (‘sunflower cataract’) seen in retroillumination.
most commonly produces a ‘sunflower cataract,’
one that is localized to the anterior or posterior
subcapsular cortex and consists of radiating
spokes (Figure 7.6).15
Traumatic cataracts, if not removed, have a
predisposition to progress to mature cataracts
(Figure 7.7), often precluding a view of the
posterior pole. Patients usually present with
decreased vision, and, rarely, intraocular inflam-
mation and elevated pressure (see Lens-induced
glaucoma, below). It is important to determine
the state of the posterior segment. The patient’s
visual potential and the presence of posterior
pathology are important factors to consider when
planning the surgical approach. If a patient pres-
ents with a total cataract, B-scan ultrasound is
used to explore the possibility of retinal tear or
detachment, choroidal rupture or occult intra-
ocular foreign body.
The degree and location of cataract formation
impacts the timing of surgical removal. The
presence of cataract does not always require sur-
gical removal. If the cataract is not significantly
dense or does not involve the central visual axis,
patients may experience relatively few symp-
toms. Refraction often improves visual acuity.
Cataracts do not necessarily progress and are not
always associated with other ocular injuries.16,17
Closed globe injuries: lens
Figure 7.7 Mature cataract following a fireworks
explosion near the right eye of an 11-year-old child.
Capsular wrinkling is present temporally. Concomitant
iris injury is visible as a D-shaped iris deformity.
The location of the cataract within the lens itself
also plays a role with respect to symptomatology.
Posterior subcapsular cataracts generally produce
more symptoms than nuclear sclerotic or cortical
cataracts of comparable density. Unless the
cataract interferes with a patient’s activities of
daily living or is associated with intraocular
inflammation, infection, or glaucoma, it is often
best managed with observation.
Preoperatively, the eye must be thoroughly
examined to determine the presence and degree
of phacodonesis, vitreous prolapse, and the state
of the posterior capsule. In general, phacoemulsi-
fication is often the most convenient route of cat-
aract removal. Great caution must be utilized in
cases of suspected zonular instability. Newer
technologies, including capsular tension rings
and capsular fi xation hooks, have greatly improved
the ability to remove these tenuous lenses via
an anterior approach. Additionally, advanced
hemodynamic parameters on new phacoemulsi-
fication units allow safe removal of traumatic
cataracts with phacoemulsification.1,18,19 A
continuous infusion can be utilized to prevent
95
 Ocular trauma
shallowing of the anterior chamber and worsen-
ing of vitreous prolapse. Capsular dyes such as
indocyanine green or trypan blue are used to
assist in performing a capsulorhexis when the red
reflex is absent. If phacoemulsification is not pos-
sible due to lens brunescence, an extracapsular
extraction may be required.
If the capsule is not intact or there is a significant
degree of phacodonesis or subluxation, other
methods of cataract removal must be considered.
The route of removal depends largely on the
experience of the surgeon. If an anterior approach
is not felt to be safe, vitreoretinal consultation is
recommended for defi nitive management. Com-
bined pars plana lensectomy and vitrectomy are
implemented with increasing frequency.20 The
infusion port should be placed away from the site
of any choroidal or retinal detachment. Perfluoro-
carbons can aid in mobilizing posteriorly dis-
located lens fragments, supporting fragments
during their removal, and protecting the retina.6
Although rarely performed, intracapsular cata-
ract surgery is an option if significant zonular
instability is present and the vitreous face is intact.
Surgeon experience plays an important role in the
decision-making process.
Primary intraocular lens implantation may be
considered after any method of cataract extrac-
tion if inflammation is well controlled and the
risk of infection is deemed to be low. The lens
may be placed in the capsular bag, the sulcus,
the anterior chamber or fi xated to the iris or
sclera. If placed in the capsular bag, the haptics
should be placed perpendicular to any zonular
defect for maximal capsular bag stabilization and
expansion.1
The timing of cataract removal depends on
many factors including the degree of inflamma-
tion, need for visual rehabilitation (monocular
patient or a child of amblyogenic age), the need
for further ocular procedures and the general
medical condition of the patient. Primary extrac-
96
tion of a cataractous lens offers many advantages:
it eliminates the source of late inflammation
and increased intraocular pressure and allows
earlier visual rehabilitation. Disadvantages in-
clude increased short-term postoperative inflam-
mation, increased risk of intraoperative bleeding
and the possibility that the cataract may not have
become visually significant.2
Young children present a unique challenge
given their risk of amblyopia. If pediatric
cataract extraction is undertaken, many factors
require consideration. One of these concerns is
the propensity for children to develop posterior
capsular opacifications relatively soon after cata-
ract removal.21,22 For this reason, a primary pos-
terior capsulotomy and anterior vitrectomy are
recommended at the time of cataract extraction
for children not mature enough to cooperate
with a YAG laser capsulotomy (typically less
than 6 years of age). Once determined to be the
treatment of choice, cataract extraction should
be expedited to minimize disruptions in physi-
ologic and anatomic ocular development.
Pediatric intraocular lens implantation is also
controversial. Of note, one study demonstrated
a 70% rate of visual acuity of >20/60 in children
with intraocular lens implantation (136 children
between 2 and 16 years of age, one child less than
2 years of age). Aphakia is generally recom-
mended for children younger than 2 years of
age,23 although intraocular implantation at
younger ages is becoming more common.
Ocular trauma with associated cataract is often
correlated with poor outcomes secondary to
posterior segment abnormalities including retinal
detachment, macular scarring, and traumatic
optic neuropathy. Between 50% and 70% of in-
jured eyes have been reported to have significant
posterior segment injuries.2,24 Preoperative
factors associated with poor visual outcomes
include an afferent pupillary defect or
iridodialysis.24

CASE EXAMPLES
Case report: traumatic cataract (Figure 7.8)
A 3-year-old girl complained to her mother of severe
pain and decreased vision in her left eye. Her family
rushed her to the emergency room for evaluation.
After initial stabilizing treatment from an ophthal-
mologist, the patient’s care was transferred to the
eye clinic for definitive evaluation and management.
Three days after the initial injury, visual acuity in the
left eye was hand motions. Slit lamp examination
revealed a Seidel negative corneal laceration of the
superotemporal cornea (black arrow, A). The anterior
lens capsule was violated with cataractous lens
material protruding through the defect. An ultra-
sound was performed which showed no intraocular
foreign body or posterior segment pathology.
A B
Included
on DVD
C D
Closed globe injuries: lens
Topical anti-inflammatories and antibiotics were ini-
tiated and the patient was scheduled for surgery.
During the surgery, trypan blue was used to stain the
anterior lens capsule to aid in visualization (B). After
the lens material was aspirated through the pre-
existing anterior capsular violation (white arrow, C),
it was evident that the penetrating injury involved a
small portion of the peripheral posterior capsule as
well (black arrow, C). The posterior capsular defect
was round and under no tension. The anterior cap-
sular break was converted into a capsulorhexis and
a one-piece acrylic intraocular lens was injected into
the capsular bag with the haptics directed away
from the pre-existing posterior capsular break.
97
 Ocular trauma
Case report: traumatic cataract (cont’d)
Because of the likelihood of future posterior capsular
opacification and the patient’s age and inability to
participate in a YAG laser capsulotomy, a posterior
capsulotomy and limited anterior vitrectomy were
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
onset, intact capsule
2. lens particle glaucoma: open angle, usually
rapid onset, violated capsule
3. phacoanaphylactic glaucoma: open angle,
variable onset, violated capsule
4. phacomorphic glaucoma: closed angle, usually
delayed onset, intact or violated capsule.
Ocular trauma is a common precipitating
factor in mature or hypermature cataracts,
although the trauma is often remote. Phacolytic
glaucoma is a secondary open angle glaucoma
resulting from leakage of lens proteins through
the intact capsule of a hypermature cataract
(Figure 7.9). Intraocular pressure increases
in response to lenticular proteins and protein-
laden macrophages occluding the trabecular
meshwork.25 The proteins are generally of
high molecular weight. Characteristic clinical
features include white patches on the anterior
lens capsule and small white collections of
inflammatory debris circulating within the
anterior chamber.26 Patients frequently pre-
sent with pain and redness in an eye with a
history of slow, progressive visual decline.
On slit lamp examination the anterior chamber
may be slightly shallowed secondary to an
enlarged anterior–posterior lens diameter, but
98
performed via the pars plana (D). The patient recov-
ered uneventfully with a final best-corrected visual
acuity of 20/20. Continued follow-up with a pediatric
ophthalmologist was arranged.
Included
on DVD
Figure 7.9 A 62-year-old female with a remote history
of trauma presented with severe pain and redness in an
eye with a longstanding history of poor vision. Vision
was light perception and intraocular pressure was
severely elevated. The video capture shows corneal
edema, anterior chamber debris with a hypopyon, and
a hypermature cataract. Cataract surgery with
intraocular lens implantation was successful, and final
visual acuity was 20/25.
unlike phacomorphic glaucoma, the anterior
chamber angle is open. Inflammatory cells
and proteinaceous debris are visible within
the aqueous but large keratic precipitates
are not typically seen. Corneal edema may
hinder slit lamp examination of the anterior
chamber.
Lens particle glaucoma can occur following
ocular trauma if the capsular bag is violated.
Intraocular pressure is elevated when lens parti-
cles exit the confi nes of the capsular bag and
mechanically block the trabecular meshwork.
Mild to moderate inflammation is typically seen.

Conversely, phacoanaphylactic glaucoma occurs
in similar situations, but is associated with a
severe, granulomatous inflammatory reaction.
Mutton fat keratic precipitates and posterior syn-
echiae are common, and a hypopyon is occasion-
ally seen. The anterior chamber angle is open in
both entities.
Phacomorphic glaucoma is a form of secondary
angle closure. A mature cataract is elongated
axially and may cause pupillary block or second-
ary angle closure if the lens apparatus is
sufficiently displaced anteriorly. Patients present
with pain and redness in an eye that demon-
strates corneal edema, a shallow anterior
chamber, and a dense cataract with increased
lens thickness on slit lamp examination.27 Mild
to moderate inflammation is often present.
Initial treatment includes anti-inflammatories
and medication to lower intraocular pressure.
A laser peripheral iridotomy may be placed in
an attempt to relieve any pupillary block that
may be present. However, cataract extraction
is the defi nitive treatment for phacomorphic
Closed globe injuries: lens
glaucoma once the initial inflammatory episode
is controlled.
For all lens-induced glaucomas, medical man-
agement is initially instituted in an effort to
decrease intraocular inflammation and pressure.
In the acute phase, intravenous osmotic agents
such as mannitol or oral osmotic agents such as
isosorbide and glycerin are utilized to lower
the pressure. Oral acetazolamide, topical beta-
blockers, topical carbonic anhydrase inhibitors,
and topical alpha-adrenergic blockers are used
to maintain a normal intraocular pressure. In
general, miotics are not recommended as they
may worsen or induce angle closure via forward
rotation of the lens–iris diaphragm. Surgical
intervention is typically deferred until inflam-
mation is controlled and intraocular pressure
decreases. However, if either persists, removal of
the cataractous lens is the defi nitive treatment
of choice. Intraocular lens implantation may be
delayed if intraocular inflammation has not been
adequately controlled, although this is rarely the
case.
99
Ocular trauma
CASE EXAMPLES
Case report: lens particle glaucoma (Figure 7.10)
A 31-year-old male presented to the emergency
room with pain in his left eye after cutting a tree with
a machete without using protective eyewear. He
recalled being hit in the face with a frond from a
palm tree. His visual acuity was 20/20 and 20/80, and
intraocular pressures were 18 and 12 without a rela-
tive afferent pupillary defect. On slit lamp examina-
tion a stellate corneal laceration was noted in the
central cornea (Seidel positive) associated with 2+
anterior chamber cell and flare. A defect in the ante-
rior lens capsule with a sectoral traumatic cataract
was also noted (A). A small amount of pigmented
material was noted on the anterior lens surface. No
foreign bodies were noted within the angle on goni-
A B
C D
100
oscopy. The patient underwent primary closure of
the corneal laceration (B). Cultures of the aqueous
did not reveal growth. Within weeks, the patient
developed elevated intraocular pressure, increased
cell and flare, and white fluffy lenticular material was
noted in the anterior chamber (C). A diagnosis of
lens particle glaucoma was made. Intensive anti-
inflammatory treatment was started and cataract
surgery was scheduled. The cataract was removed
the next day, topical steroids were continued, and
his pressure quickly returned to the normal range.
On the final follow-up visit, a well-centered intra-
ocular lens was present (D) and visual acuity was
20/20.

SUMMARY
1. Lens subluxation implies a partial dehiscence
of zonules whereas lens dislocation is caused
by complete zonular dehiscence.
2. Phacodonesis is a pathologic instability of the
lens caused by diffuse zonular damage.
3. Traumatic lens instability is often accompa-
nied by an asymmetrically deep anterior
chamber, iridodonesis, an eccentric pupil
shape, or vitreous prolapse.
4. The urgency of traumatic cataract removal
depends on the presence of visual symptoms,
inflammation, elevated intraocular pressure,
and ability to follow up.
5. Removal techniques for traumatic cataracts
vary depending on zonular stability, presence
of vitreous prolapse, cataract density, and
surgeon preference.
6. Traumatic lens sequelae may occur years after
the initial injury.
7. Traumatic lens injuries can induce glaucoma
via multiple open and closed angle mecha-
nisms, but lens removal is the defi nitive man-
agement for each entity.
REFERENCES
1. Mian SI, Azae DT, Colby K. Management of traumatic
cataracts. Int Ophthalmol Clin 2002;42:23–31.
2. Kuhn F, Mester V. Anterior chamber abnormalities
and cataract. Ophthalmol Clin North Am 2002;15:
195–203.
3. Lamkin JC, Azar DT, Mead MD, Volpe NJ. Simultaneous
corneal laceration repair, cataract removal, and posterior
chamber intraocular lens implantation. Am J Ophthalmol
1992;113:626–631.
4. Jones LD, Sampat V, Hero M. Indirect trauma causing
dislocation of the crystalline lens: a case report. Eur J
Ophthalmol 2003;13:91–92.
5. Loo AV, Lai JS, Tham CC, Lam DS. Traumatic subluxation
causing variable position of the crystalline lens. J Cataract
Refract Surg 2002;28:1077–1079.
Closed globe injuries: lens
6. Marcus DF, Topping TM, Frederick AR. Vitreoretinal
management of traumatic dislocation of the crystalline lens.
Int Ophthalmol Clin 1995;3591:139–150.
7. Berinstein DM, Gentile RC, Sidoti PA, et al. Ultrasound
biomicroscopy in anterior ocular trauma. Ophthalmic Surg
Lasers 1997;28:201–207.
8. Ozdal MPC, Mansour M, Deschenes J. Ultrasound
biomicroscopic evaluation of the traumatized eye.
Eye 2003;17:467–472.
9. Sathish S, Chakrabarti A, Prajna V. Traumatic subconjunctival
dislocation of the crystalline lens and its surgical
management. Ophthalmic Surg Laser 1999;30:684–686.
10. Yurdakul NS, Ugurlu S, Yilmaz A, Maden A. Traumatic
subconjunctival crystalline lens dislocation. J Cataract Refract
Surg 2003;29:2407–2410.
11. Ellant JP, Obstbaum SA. Lens-induced glaucoma.
Doc Ophthalmol 1992;81:317–338.
12. Wolter JR. Coup-contrecoup mechanism of ocular injuries.
Am J Ophthalmol 1963;56:785–796.
13. Weidenthal DT, Schepens CL. Peripheral fundus changes
associated with ocular contusion. Am J Ophthalmol
1966;62:465–477.
14. Shingleton BJ, Hersch PS, Kenyon KR, eds. Eye Trauma.
St. Louis, MO: Mosby-Year Book; 1991; Ch. 11, Lens injuries,
pp. 126–135.
15. Trevor-Roper PD. The eye and its disorders. The lens.
Int Ophthalmol Clin 1974;14:485–520.
16. Yasukawa T, Kita M, Honda Y. Traumatic cataract with a
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
by blunt ocular trauma. J Cataract Refract Surg
1997;23:139–140.
18. Cionni RJ, Osher RH. Management of profound zonular
dialysis or weakness with a new endocapsular ring designed
for scleral fixation. J Cataract Refract Surg 1998;24:1299–1306.
19. Menapace R, Findl O, Georgopoulos M, Rainer G, Vass C,
Schmetterer K. The capsular tension ring: designs,
applications, and techniques. J Cataract Refract Surg
2000;26:898–912.
20. Chaudhry NA, Belfort A, Flynn HW, Tabandeh H, Smiddy WE,
Murray TG. Combined lensectomy, vitrectomy and scleral
fixation of intraocular lens implant after closed-globe injury.
Ophthalmic Surg Lasers 1999;30:35–81.
21. Chrousos GA, Parks MM, O’Neill JF. Incidence of chronic
glaucoma, retinal detachment and secondary membrane
surgery in pediatric aphakic patients. Ophthalmology
1984;91:1238–1241.
101
 Ocular trauma
22. Keech RV, Cibis-Tongue A, Scott WE. Complications after
surgery for congenital and infantile cataracts. Am J
Ophthalmol 1989;108:136–141.
23. Krishnamachary M, Rathy V, Gupta S. Management of
traumatic cataract in children. J Cataract Refract Surg
1997;23:681–687.
24. Greven CM, Collins AS, Slusher MM, Weaver RG. Visual results,
prognostic indicators, and posterior segment findings
following surgery for cataract/lens subluxation-dislocation
102
secondary to ocular contusion injuries. Retina
2002;22:575–580.
25. Filipe JC, Palmares J, Delgado L, Lopes JM, Borges J, Castro-
Correia J. Phacolytic glaucoma and lens-induced uveitis.
Int Ophthalmol 1993;17:289–293.
26. Epstein DL. Diagnosis and management of lens-induced
glaucoma. Ophthalmology 1982;89:227–230.
27. De Leon-Ortega JE, Girkin CA. Ocular trauma-related
glaucoma. Ophthalmol Clin N Am 2002;15:215–223.

Closed globe injuries:
posterior segment
John J. Miller, Krista D. Rosenberg
INTRODUCTION
Contusive ocular injury may damage posterior
segment structures by multiple mechanisms. In-
jury severity varies widely from self-limited peri-
pheral commotio retinae to vision-threatening
retinal detachment. The vitreoretinal interface
plays a vital role in the pathophysiology of most
retinal injuries. Retinal detachment is often the
fi nal common pathway for traumatic disruption
of the pars plana, vitreous base, or retina. In this
chapter we will discuss the epidemiology, patho-
physiology, examination, and treatment of con-
tusive posterior segment injury. Many of the
entities described here can occur with open globe
injuries; however, in these cases repair of the
globe violation remains the primary goal of initial
management (see Chapter 11). Treatment of
coexisting posterior segment injuries following
primary closure of an open globe injury typically
requires management by a vitreoretinal special-
ist. Such complex injuries are outside the scope of
this chapter.
EPIDEMIOLOGY
Much of the reported epidemiologic information
regarding contusive posterior segment injury
focuses on traumatic retinal detachment, a fi nal
common pathway for most posterior segment
injuries. Traumatic retinal detachments account
for 10% and 19% of all phakic retinal detach-
ments.1–4 Phakic retinal detachments have been
noted to have a bimodal distribution and several
distinct clinical characteristics:
8
1. Trauma contributes to the peak incidence in
younger years (20–29 years of age).
2. 80% of traumatic detachments occur prior to
the age of 40.
3. Men outnumber women in traumatic detach-
ment (78% vs. 22%).
4. Non-traumatic detachments contribute to the
second peak incidence between the ages of 60
and 69.
5. 75% of non-traumatic detachments occur
after the age of 39.
The increased risk of non-traumatic detachment
in myopic patients is well established. While
some studies were unable to reach a conclusion
regarding the role of myopia in traumatic detach-
ments,5 others concluded that myopia was indeed
a risk factor. While 3% of the general population
has myopia of 2.5 diopters or greater, 28% of
traumatic detachments have this degree of
myopia or more. Assuming that myopes have a
similar trauma incidence as hyperopes and
emmetropes, the incidence of traumatic retinal
detachments in myopes may be as much as nine
times greater.
Trauma, in addition to proliferative diabetic
retinopathy and retinal tear, is a leading cause of
vitreous hemorrhage.6–8 Vitreous hemorrhage
occurs in approximately 19% of all posterior
segment injuries9 and is most commonly associ-
ated with contusive (66%), projectile (25%),
and lacerating (9%) injuries. Trauma is the most
common cause of unilateral vitreous hemorrhage
in patients under 40 years of age, usually occur-
ring in males.
Traumatic choroidal ruptures have been
reported in 4–10% of contusive ocular
103
 Ocular trauma
injuries.10,11 Closed globe trauma from motor
vehicle accidents, assault,12 sports-related activi-
ties,13 forceps delivery,14 and paintball injuries15
are all reported causes of choroidal rupture.
PATHOPHYSIOLOGY
Contusive injuries to the eye cause deformation
of normal ocular architecture and, at times, dis-
ruption of the vitreoretinal interface. The vitre-
ous most tightly adheres to the retina at the
vitreous base, a band of condensed vitreous that
straddles the ora serrata 360 degrees (Figure
8.1). Firm vitreoretinal adherence is also present
along the retinal vasculature and at the optic
nerve head. Vitreous hemorrhage is caused by
traction or shearing of a normal or abnormal
retinal vessel, frequently when traumatic separa-
tion of the vitreous occurs. The rapid tractional
Pars plan Ora serrata
Vitreous base
insertion
Retina
Figure 8.1 Anatomical interaction of the vitreous
base and ora serrata. The vitreous base extends
approximately 2 mm anterior to the ora serrata and 2–
4 mm posteriorly. This tight interface plays a major role
in the pathophysiology of traumatic retinal breaks and
detachments.
104
forces on the vitreoretinal interface that shear
vessels may also disrupt the normal retinal archi-
tecture (e.g. macular hole).
Weidenthal and Schepens described the mech-
anisms of traumatic tear formation by studying
pig eyes subjected to pellet gun injury. Most
peripheral retinal damage occurred from rapid
equatorial scleral expansion and rotation, while
the vitreous and retina are pulled away from the
underlying pigment epithelium.16 Contusive
ocular trauma can disrupt normal vitreoretinal
adhesions and may cause retinal dialyses, giant
retinal tears, horseshoe retinal tears, or tears in
the nonpigmented pars plana epithelium. Tears
in the nonpigmented pars plana epithelium are
much less common and are caused by traction at
the anterior aspect of the vitreous base. A retinal
dialysis occurs when vitreous base traction causes
a disinsertion of retina from the nonpigmented
pars plana epithelium at the ora serrata, rather
than a tear within the retina. The vitreous
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
vitreoretinal adherence posterior to the ora
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
scenario commonly occurs in older patients with
an evolving posterior vitreous detachment.
A few generalizations can be made regarding
the origins of retinal detachments and their pos-
sible relationship to trauma. Most retinal dialy-
ses and giant retinal tears are related to trauma,
although some develop without trauma. Detach-
ments related to superior or nasal dialyses, pars

plana tears, vitreous base avulsions, and necrotic
retinal holes may be assumed to be of traumatic
origin, even if the history of trauma is remote or
not recalled by the patient. Conversely, most
horseshoe tear-related detachments are not asso-
ciated with contusive trauma.
Choroidal ruptures occur when contusive
forces overcome the inelastic nature of Bruch’s
membrane and the retinal pigment epithelium
(RPE), causing a tear in these tissues. Histo-
pathologic evidence reveals an intact overlying
retina with variable fibroglial scarring.17
EXAMINATION AND DIAGNOSIS
Clinical examination in the setting of ocular
trauma must be tailored to the clinical situation.
Contusive trauma stresses the vitreoretinal inter-
face and vitreous base, increasing the risk of vit-
reoretinal interface separation. Such a disruption
may lead to more sinister posterior segment
pathology. During the post-traumatic period,
every patient should receive a complete ocular
examination, including scleral depression with
ophthalmoscopic viewing of the ora serrata and
vitreous base. However, examination in the acute
setting may be limited by the severity of injury,
patient discomfort, and clarity of ocular media.
In lucid patients, best-corrected visual acuity
is measured with the Snellen chart. In an emer-
gency room setting, a Rosenbaum near card will
suffice. Careful opening of the lids with Des-
marres lid retractors may be necessary if the
patient is unable to open the eye due to lid edema
or hemorrhage. Determination of pupillary light
reaction and evaluation for a relative afferent
pupillary defect should be performed on every
patient, regardless of consciousness.
Examination of the anterior segment prior to
further manipulation prevents iatrogenic injury.
Corneoscleral integrity and anterior chamber
depth should be determined initially to rule out
Closed globe injuries: posterior segment
an open globe. Examination considerations for a
potential open globe are covered in Chapter 11.
Any hyphema should be noted. Intraocular pres-
sure should be measured after confi rmation of
globe integrity.
After the pupils have been pharmacologically
dilated, evaluate the lens for traumatic lens opac-
ities (cataract) and traumatic lens instability
(phacodonesis). Both indicate significant ocular
trauma and often coexist with disruption of the
vitreous base and retina. With the slit lamp bio-
microscope, examination of the anterior vitreous
just posterior to the lens yields clues to vitreo-
retinal integrity. The presence of liberated retinal
pigment epithelial cells and pigment-containing
macrophages (also known as tobacco dust or Included
on DVD
Schafer’s sign) indicates a probable retinal break.
These pigmented cells gain access to the anterior
vitreous cavity through defects in the retina. The
presence of blood (vitreous hemorrhage) may
indicate a disruption of the ciliary body, retina,
or retinal vasculature.
Indirect ophthalmoscopy should be performed
bilaterally in a systematic fashion. Examine the
optic disc, macula, vessels, and the complete
periphery. Special attention should be paid to
whitened areas of retina indicative of commotio
retinae and the presence of subretinal hemor-
rhage, which may herald a choroidal rupture. In
the presence of intraocular hemorrhage or cor-
neoscleral compromise, scleral depression should
be deferred until structural stability is confi rmed.
However, scleral depression of the retinal periph-
ery to the vitreous base and ora serrata must be
performed at some point in the post-traumatic
period.
If patient discomfort or media opacities prevent
complete viewing of the ocular fundus and
periphery, B-scan ultrasonography should be
used to examine the posterior segment. Ultra-
sound, in the hands of trained ophthalmic tech-
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
most common retinal manifestation of contusive
ocular injury.18 Confluent geographic areas of
whitened retina most commonly appear in the
mid-periphery and less commonly in the macula
(Figure 8.3). Commotio retinae involving the
macula is also known as Berlin’s edema. It may
occur following coup or countercoup injuries.
Histopathologic studies in animals19,20 and in
outer segments and retinal pigment epithelium.
Intraretinal pigment migration and, in severe
cases, thinning of the outer retinal layers occurred
following the acute phase. In vivo studies of
acute commotio retinae by fundus reflection
densitometry22 and optical coherence tomogra-
phy23 also identified photoreceptor outer segment
and retinal pigment epithelium (RPE) damage.
Fluorescein angiography performed 30 minutes

106

following contusive ocular trauma revealed stain-
ing of the RPE underlying the retinal whitening
but no leakage from retinal vessels. These results
further suggest photoreceptor outer segment and
retinal pigment epithelium damage.24
Acute vision loss may occur when commotio
retinae involves the macula, or it may be visually
asymptomatic if only the retinal periphery is
involved. Vision typically improves as retinal
whitening resolves. An experimental study of
photoreceptor function reported recovery of
normal function within 3 months. The prognosis
is good for extrafoveal and mild trauma. However,
vision loss may be permanent if the fovea is
damaged. While 60% of patients in a prospective
study had complete recovery of vision within
weeks of injury, the remaining 40% were left
with macular damage and varying degrees of
permanent vision loss. Long-term sequelae may
also include RPE changes and pigment migra-
tion. Such pigment migration in the retinal
periphery may mimic the bone spicules of reti-
nitis pigmentosa. Although there is no known
treatment for commotio retinae, the frequency
of concomitant ocular injury warrants close
observation and thorough examination.
Traumatic vitreous hemorrhage
Common symptoms of vitreous hemorrhage
include sudden, punctate, or web-like floaters
and decreased visual acuity. Sometimes patients
will literally report seeing red. While the density
and location of the hemorrhage primarily deter-
mine visual acuity, a small amount of blood can
cause a significant decrease in vision. Thompson
and Stoessel reported that although 0.832 micro-
liters of diffuse vitreous blood caused no decrease
in vision, 10 microliters of vitreous blood can
decrease vision to hand motions or worse in a
phakic eye model. Furthermore, visual acuity
measured in light was worse than acuity mea-
sured in dark, owing to intraocular light scatter.25
Closed globe injuries: posterior segment
It is important to determine, if possible, the
underlying cause of the vitreous hemorrhage,
as treatment may vary. The most frequent
causes of vitreous hemorrhage associated with
trauma are posterior vitreous detachment, retinal
detachment, retinal tear, and pre-existing prolif-
erative diabetic retinopathy.26–28 The presence of
vitreous hemorrhage in an infant or child should
alert the physician to the possibility of abuse.
In this setting, photographic documentation
and further investigation with a pediatrician is
vital.
Acute vitreous hemorrhage undergoes rapid
clot formation and appears red with distinct
borders. Slowly, the blood begins to diffuse
throughout the vitreous within the fi rst day to
week after the initial hemorrhage.29,30 In lique-
fied vitreous or a previously vitrectomized eye,
blood clears from the vitreous cavity more rapidly
than in an eye with formed vitreous. 31 As red
blood cells are phagocytosed and hemoglobin is
broken down, the hemorrhage takes on a yellow-
brown hue as early as 10 days. The vitreous
gel in an infant eye is more formed than in an
adult. Therefore, neonatal vitreous hemorrhages
may sequester within Cloquet’s canal, remain
concentrated for long periods, and reabsorb
slowly. 32
If dense vitreous hemorrhage precludes ade-
quate ophthalmoscopic retinal viewing, ultra-
sound provides an alternative examination.
Echography most effectively determines the
presence or absence of intraocular foreign
bodies, eyewall deformities, or retinal detach-
ments. Mild to moderate vitreous hemorrhage
appears as mobile opacities on B-scan and as
low-amplitude spikes on A-scan, while marked
vitreous hemorrhage displays denser echoes on
B-scan and higher amplitude spikes on A-scan.
If hemorrhage accumulates under the posterior
hyaloid, the increased reflectivity along the
hyaloid surface may mimic a retinal detachment.
107
 Ocular trauma
However, positional shifting of the hemorrhage
distinguishes it from the retina. 33 A-scan and B-
scan ultrasound examination of eyes with dense
vitreous hemorrhage often successfully identifies
retinal detachments, but echographic detection
of retinal tears is challenging. 34 Among eyes with
dense vitreous hemorrhage, Rabinowitz reported
all retinal detachments (30 eyes) were identified
correctly with an 18.9% false-positive rate,
whereas only 44% of retinal tears were identi-
fied.8 In contrast, DiBernardo reported 10 of 11
(91%) small retinal tears associated with vitre-
ous hemorrhage were diagnosed correctly by
ultrasound. 35 While ultrasonography remains
largely operator-dependent and has limitations
when ruling out small tears, it detects serious
posterior segment pathology that would other-
wise remain hidden until hemorrhage dissolu-
tion or surgical exploration occurred.
In a closed globe injury with vitreous hemor-
rhage but no retinal detachment or retinal break,
patients are observed to allow spontaneous clear-
ance of the hemorrhage. 36 Bed rest and head
elevation are generally recommended to allow
gravitational settling of the hemorrhage. Re-
examination for hemorrhage resolution or retinal
detachment should be scheduled within 2 weeks
of the initial evaluation. No topical medications
have proven beneficial to speed the clearing of
isolated vitreous hemorrhages.
In eyes without a pre-existing vitreous detach-
ment, a posterior vitreous detachment com-
monly develops in the weeks following contusive
trauma. This independently increases the risk of
subsequent retinal tear or detachment, making
follow-up examinations important. If the view
remains limited, the treating ophthalmologist
should perform serial ultrasound screening for
posterior segment pathology. If vitreous hemor-
rhage remains for several weeks or if potential
retinal pathology is detected, vitreoretinal con-
sultation should be sought.
108
Vitreoretinal surgeons perform vitrectomy for
traumatic vitreous hemorrhage only if the hem-
orrhage shows no sign of resolution. In an other-
wise normal eye with normal serial ultrasounds,
vitrectomy can be delayed depending on the
visual acuity in the fellow eye and the functional
status of the patient. Most surgeons will wait at
least 2–3 weeks for a posterior vitreous detach-
ment to develop and will intervene surgically
only if the hemorrhage persists for more than
2–3 months. 37
If a retinal tear is identified and vitreous hem-
orrhage precludes laser demarcation, vitrectomy
is often performed within 2 weeks of presenta-
tion, as progression to retinal detachment typi-
cally occurs within that period. In the setting of
traumatic vitreous hemorrhage, patients with a
history of retinal detachment in the contralateral
eye should be considered for earlier vitrectomy. 38
In the presence of retinal detachment, early vit-
rectomy should be performed, typically within
1 week. Among a survey of vitreoretinal sur-
geons, surgery for vitreous hemorrhage with
retinal tear was performed at a mean 1.7 weeks
and vitreous hemorrhage with retinal detach-
ment at 1 week.
Children in the amblyopic age range present a
therapeutic challenge. It is imperative to watch
children with vitreous hemorrhage closely until
resolution or until the decision for surgery is
made. In infants, deprivation amblyopia may
occur within weeks of a dense vitreous hemor-
rhage. 39 Mohney reported that an increase in
axial length (averaging 3.45 mm more than the
unaffected fellow eye) can occur within weeks
of vitreous hemorrhage onset.40 Such asymmet-
ric axial lengths may cause anisometropia as
great as 11 diopters. The pediatric patient’s age
and hemorrhage density guide the timing of
vitrectomy. Patients less than 1 year old
develop myopic anisometropia more readily
than older patients.41 Typically, surgeons perform

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
blood cells and may be classified into ghost cell,
hemolytic, or hemosiderotic glaucomas. Long-
standing vitreous hemorrhage may also cause
retinal damage through chronic iron toxicity.42
Using radiolabeled 60Fe in rabbit eyes, Regnault
reported 25% and 29% of iron was still present
in ocular tissues 2 months after hemoglobin or
whole blood injection, respectively. 30 Breakdown
of erythrocyte cell membranes can sometimes
cause synchysis scintillans (also known as chol-
esterolosis bulbi). This collection of colorful
cholesterol crystals may develop within the vit-
reous cavity or anterior chamber but is rarely
visually significant (Figure 8.4). Vitreous hemor-
rhage may also stimulate fibrovascular pro-
liferation with subsequent tractional retinal
detachment; however, this more commonly
occurs in eyes with penetrating injuries.43,44
Traumatic macular hole
The fovea is avascular and lacks structural
support from the inner retinal layers. Acute con-
tusive injury in an eye without a pre-existing
posterior vitreous detachment may cause a full-
thickness macular hole at the time of impact.
Although the mechanism of formation is incom-
Closed globe injuries: posterior segment
Figure 8.4 Synchysis scintillans following vitreous
hemorrhage.
pletely understood, surface traction at the vit-
reoretinal interface during equatorial expansion
of the globe and flattening of the posterior pole
likely initiates hole formation.45 Vitreomacular
traction in the setting of a delayed, trauma-
induced posterior vitreous detachment may
induce macular hole formation days to weeks
following trauma.46 Reported causes of traumatic
macular hole include:
1. contusive ocular trauma47–49
2. electrical injury50,51
3. Nd:YAG laser52,53
4. thermal laser.54,55
Overall, trauma has been reported to cause
nearly 10% of all full-thickness macular
holes.56,57
Acute traumatic macular holes are typically
less than 1/2 disc diameter in size, although
chronic traumatic holes may grow larger.58 The
holes may be round or oval in shape. Vision typi-
cally remains 20/400 or better. Aside from a
history of ocular trauma, the more common
idiopathic macular holes may be clinically indis-
tinguishable from traumatic macular holes.
109
 Ocular trauma
Traumatic macular holes have a variable natural
history. Spontaneous closure of traumatic
macular holes with improvement in visual acuity
is well documented.59–65 Small case series ranging
from 6 to 18 eyes report spontaneous closure
rates of 10–67%. The overall incidence of spon-
taneous closure cannot be determined without
observation of a large number of patients.
However, those eyes that had spontaneous
closure shared some clinical features: small hole
size (0.1–0.2 disc diameters), no posterior vitre-
ous detachment, and no cuff of subretinal fluid.
Spontaneous closure occurred within 1 month
in 35% and within 9 months in all reported
cases. Final visual acuity was 20/40 or better in
55% and 20/100 or better in 70%.
Although many traumatic macular holes may
close spontaneously, surgical intervention offers
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
paintball shooting. The paintball struck the left lower
eyelid (A) causing immediate pain and decreased
vision. Initial visual acuity was 20/200 in the involved
left eye. The left pupil was enlarged and sluggish,
but no relative afferent pupillary defect was present.
Anterior segment examination revealed conjunctival
injection, a small hyphema, and mild traumatic
mydriasis. Posterior segment examination revealed a
small macular hole and a large inferior retinal tear
110
improved hole closure rates when compared
with observation alone. However, critics of
surgery performed in the early post-traumatic
period cite similar fi nal visual acuity outcomes
in patients observed versus those repaired surgi-
cally. While delaying surgery for a few months
to assess for spontaneous closure has been advo-
cated by some, others claim that early surgery
offers the best chance for visual recovery.
Appropriate referral to a vitreoretinal special-
ist for defi nitive management is indicated. Repair
of traumatic macular holes includes pars plana
vitrectomy, posterior hyaloid dissection, fluid-
gas exchange, and long-acting intraocular gas
tamponade. Anatomic closure rates following
vitrectomy and gas tamponade range from 93%
to 100%. Final visual acuity improved to 20/50
or better in 35–79%.66,67
(white arrow, B) with associated hemorrhage. The
patient underwent a scleral buckle procedure, pars
plana vitrectomy with posterior hyaloid dissection
and peeling of the internal limiting membrane,
endolaser, and injection of C3F8 gas for intraocular
tamponade. (C) Before and after ocular coherence
tomography scans reveal resolution of the macular
hole. (D) Despite an excellent anatomic result, visual
acuity remained 20/200.
 Closed globe injuries: posterior segment

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

111
 Ocular trauma
Figure 8.6 Multifocal choroidal rupture involving the
fovea of a young child.
which the choroidal rupture develops. Multiple
rupture sites have been reported in 19–37% of
all eyes with ruptures, and 50–66% of ruptures
involve the macula. As with most traumatic inju-
ries, males are more commonly affected.
Immediate vision loss occurs with direct
involvement of the macula or associated serous
detachment, retinal edema, or hemorrhage.74–76
In most cases, visual acuity recovers as the fluid
or hemorrhage resolves. While patients may
complain of a scotoma, the site of choroidal
rupture does not always correlate with visual
field defects.77 Furthermore, the size of the field
defect may appear larger than clinical examina-
tion would predict, suggesting overlying retinal
damage is more extensive than the rupture site
itself.78 Rupture location often determines fi nal
visual outcome with foveal involvement typically
causing permanent visual acuity loss. Neverthe-
less, some patients with subfoveal rupture retain
20/20 vision.
Epiretinal membrane formation,79 serous
retinal elevation,80 or choroidal neovasculari-
zation81,82 may cause delayed-onset vision loss.
112
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
hemorrhage and fluid. Choroidal neovasculariza-
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
of CNVM since asymptomatic extrafoveal or
peripapillary membranes escape presentation to
an ophthalmologist. Secretan and colleagues
reported that choroidal neovascularization was
more likely to develop from ruptures closer to
the foveal center and with greater rupture length.
The majority of eyes (81.2%) in their study
developed a neovascular membrane within 1
year of injury.73
Fluorescein angiography confi rms the presence
of a presumed CNVM. Choroidal ruptures
appear as window defects without appreciable
leakage. If choroidal neovascularization is
present, the lesion will typically hyperfluoresce
early and leak late. The presence of blood may
interfere with clinical examination or fluorescein
angiography, obscuring the presence of choroidal
neovascularization. Indocyanine green (ICG)
angiography is a useful alternative for identifying
and characterizing choroidal ruptures and asso-
ciated choroidal neovascularization that may be
obscured by overlying hemorrhage.84–86
No treatment exists for a traumatic choroidal
rupture. Regular funduscopic examination

should be performed every 6 months for the fi rst
2 years following the injury to detect the devel-
opment of choroidal neovascularization. Careful
attention for the development of CNVM is war-
ranted for ruptures longer than 4000 μm or
within 1500 μm of the foveal center. For these
larger ruptures, long-term follow-up is recom-
mended since choroidal neovascularization has
been reported to occur up to 37 years following
the injury.87 The treating ophthalmologist should
instruct patients experiencing a decline in vision
or metamorphopsia to return immediately for a
dilated examination.
Therapeutic options for CNVM include
observation, photocoagulation,87 photodynamic
therapy,89,90 or submacular surgical removal. The
use of drugs which target vascular endothelial
growth factor (VEGF) is a new modality that is
being investigated. Since they are distant from
CASE EXAMPLES
Case report: choroidal rupture with CNVM (Figure 8.7)
A 32-year-old male presented to the emergency
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-
Closed globe injuries: posterior segment
the macula, membranes nasal to the disc are
often observed. Occasionally, spontaneous invo-
lution occurs.
Visual prognosis depends on the rupture size,
location and secondary complications (particu-
larly CNVM). Hemorrhage or edema may affect
vision in the acute setting, but presenting visual
acuity is not a prognostic factor. Visual acuity
typically recovers in eyes with non-foveal rup-
tures. Greater rupture length portends a poor
visual outcome, owing to the risk of choroidal
neovascularization. Close proximity to the fovea
also heralds poor visual acuity from damaged
macular photoreceptors. Furthermore, multiple
rupture sites indicate severe ocular trauma, likely
with concomitant ocular injuries. Associated
injuries such as macular hole, pigment epithelial
atrophy, commotio retinae, or optic atrophy may
adversely affect visual recovery.
A
113
 Ocular trauma
Case report: choroidal rupture with CNVM (cont’d)
ations and an epiretinal membrane were present
nasal to the fovea. Of note, the superotemporal
portion of the choroidal rupture was associated with
an elevated subretinal lesion surrounded by a cuff of
subretinal fluid (A), consistent with a choroidal
neovascular membrane (CNVM). Fluorescein angio-
graphy (FA) was obtained. Early frames of the FA
revealed early hyperfluorescence of the choroidal
rupture and CNVM as well as mottled hyperfluo-
rescence in the area of pigmentary alteration in the
nasal macula (B). Late frames reveal leakage from
B C
Suprachoroidal hemorrhage
Traumatic suprachoroidal hemorrhage, or hem-
orrhagic choroidal detachment, occurs when
blood accumulates within the potential space
between the choroid and the sclera. This poten-
tial space extends from the scleral spur anteri-
orly to the optic nerve posteriorly. The choroid
is anchored at the vortex veins, leading to the
characteristic dome-shaped appearance of cho-
roidal detachments. Hemorrhage occurs follow-
ing rupture of the long or short posterior ciliary
arteries91–93 or ciliary body vessels. 94 Hemor-
114
the CNVM and staining of the nasal macula (C).
The diagnosis of choroidal rupture-associated
CNVM was made. The patient was given multiple
therapeutic options. Given the proximity of the
lesion to the fovea and the patient’s desire to
avoid laser treatments, an intravitreal injection of
an anti-VEGF agent was given. On follow-up, the
CNVM resolved completely with resolution of
the patient’s metamorphopsia. The visual acuity
remained unchanged.
rhagic choroidals most commonly occur with
penetrating ocular injuries95,96 and should raise
the suspicion for an open globe when encoun-
tered. Less commonly, sudden decompression of
the globe during contusive trauma can create a
similar picture.97
Traumatic suprachoroidal hemorrhage may
present with a shallow or flat anterior chamber,
with or without expulsion of intraocular con-
tents. Pain and elevated intraocular pressure
often result if the globe remains intact. Fundo-
scopic examination reveals dark, dome-shaped
 Closed globe injuries: posterior segment

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
the retina and choroid, thereby causing retrac-
tion of these two tissues together, while the
underlying sclera remains intact.
The extent of the chorioretinal damage depends
on the size, velocity, and proximity of the pro-
jectile to the globe. Fibrous proliferation during
the healing process anchors the retinochoroidal
margin to the underlying sclera. Surrounding
pigmentation occurs within days to weeks. After
associated hemorrhage or edema clears, the
affected area appears scarred and atrophic with
serrated, pigmented margins. The full-thickness
chorioretinal break may reveal underlying bare
sclera or secondary fibrotic tissue (Figure 8.9).
Additionally, preretinal gliosis may occur at sites
distant to the chorioretinal rupture. Despite the
intensity of the injury, the overlying posterior
hyaloid face may not be disrupted. In fact, the
vitreous often strongly adheres to the rupture
edges. Indirect trauma, including posterior cho-
roidal ruptures and macular damage, commonly
occurs simultaneously with sclopetaria. Con-
comitant retinal tears may also be present,
making a complete peripheral retinal exam
necessary.
Choroidal and retinal hemorrhage is often
present initially. Thickened, edematous retinal
margins may give the impression of a retinal
detachment or tear. Ultrasonography or optical
116
Figure 8.9 Sclopetaria is seen in a young patient who
suffered a gunshot wound that passed through the
orbit without direct contact with the globe. Severe
fibrosis and loss of retinochoroidal architecture follows
the course of the projectile through the orbit.
coherence tomography can be helpful in differ-
entiating between chorioretinal edema and a
true retinal detachment. Damage to the retinal
circulation outside the ruptured areas causes
visual field defects distant to the areas of scar-
ring. Visual field testing often shows larger
defects than would be predicted by sclopetaria
size alone.
Patients may experience acute loss of vision
depending on the location of the injury. Final
visual acuity of 20/20 has been reported in
several cases. If the macula is involved, profound
and permanent visual loss typically occurs. If the
macula remains uninvolved, related traumatic
injuries primarily cause visual loss.
Since the high-velocity nature of the injury
seals the retina and choroid to the underlying
sclera, surgical intervention is rarely required.
Retinal detachment uncommonly follows sclop-
etaria, making prophylactic cryotherapy, laser
photocoagulation, or scleral buckling unneces-
sary. Typically, treatment consists of observa-
tional management with continued long-term
follow-up to screen for future post-traumatic

complications such as angle recession glaucoma,
vitreous hemorrhage, or retinal detachment.
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
should be referred to a vitreoretinal specialist so
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
for traumatic detachments often will vary
depending on the underlying cause.
Retinal dialysis
Retinal dialysis is a disinsertion of the retina
from the nonpigmented pars plana epithelium at
the ora serrata. The disinserted retina remains
attached to the vitreous base (Figure 8.10). Dial-
ysis has been reported to cause 7% of rhegmato-
genous retinal detachments. Trauma, myopia,
and congenital weakness of the peripheral retina
may all contribute to the development of a dialy-
sis. Myopia was present in 11% of patients in two
different large series,119,120 and a heritable weak-
ness of the peripheral retina has been suggested
as an independent cause.121,122 However, clinical
evidence has shown trauma to be the primary
cause in the majority of cases.123–125 In a series of
586 detachments, a history of trauma was
reported in 87% of superonasal dialyses and in
61% of inferotemporal dialyses.
The most common location for dialyses of all
origins is the inferotemporal quadrant. Embryo-
logic studies have shown that the inferotemporal
quadrant contains the weakest peripheral retina
because the temporal pars plana grows more
rapidly than the temporal peripheral retina,
Closed globe injuries: posterior segment
Retinal dialysis
Pars plan Ora serrata
Vitreous base
insertion
Retina
Figure 8.10 An intact vitreous base associated with a
retinal dialysis allows little fluid to enter the subretinal
space and inhibits proliferative vitreoretinopathy,
leading to a slowly progressive retinal detachment or
even spontaneous healing.
thereby inducing a tractional force that weakens
the retina in this region.126 Furthermore, the ora
serrata is the thinnest portion of the retina. Tem-
porally, there is little protection from the nasal
bridge or bony orbital rim. Relatively weak retina
with relatively less bony protection may predis-
pose to inferotemporal dialysis, even with minor
trauma as an initiating factor. Between 22% and
68% of unilateral inferotemporal dialyses have
been associated with a defi nite history of prior
trauma. The most common location of trauma-
related dialyses is the superonasal quadrant.127,128
This underscores the importance of countercoup
injuries since the inciting injury typically is
directed at the inferotemporal quadrant, the
least protected area of the eye.
Similar to detachments associated with pars
plana tears, detachments associated with retinal
dialysis typically have few symptoms. They may
117
 Ocular trauma
remain undiagnosed for long periods of time and
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
and prevents large amounts of vitreous fluid
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
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-
cedent trauma and account for approximately
25% of all tears in several published series. Many
non-traumatic giant tears are associated with
myopia. Giant tears have been reported in 16%
of traumatic retinal detachments, of which the
majority of eyes were emmetropic.130–133 Based
on this epidemiologic information, there appear
to be two primary mechanisms in the formation
of giant tears: contusive ocular trauma to an
otherwise normal eye and spontaneous giant tear
formation in the myopic eye. In reality, a spec-
trum of scenarios produce giant tears, with
varying degrees of predisposing myopia com-
bined with a varying severity of precipitating
trauma. Demographically, trauma-induced giant
retinal tears occur most commonly in young
males. In a study of 586 traumatic and non-
traumatic retinal detachments, a history of
trauma was elucidated in 67% of patients with
giant tears.
Giant retinal tears, like other traumatic retinal
breaks related to contusive trauma, are typically
located in the inferotemporal or superonasal
quadrants. The duration of time from contusive
eye trauma to diagnosis of retinal detachment is
118
Pars plan Ora serrata
Vitreous base
insertion
Retina
Figure 8.11 Horseshoe tears occur along the vitreous
base in the presence of a posterior vitreous
detachment. Giant retinal tears occur when the tear
extends along the posterior edge of the vitreous base
(hatched line) for >3 clock hours.
usually a month or less. By comparison, giant
retinal tears related to penetrating ocular trauma
often present with detachment more than a
month later, owing to delayed posterior vitreous
detachment or proliferative vitreoretinopathy.
Almost all giant tears are associated with a
posterior vitreous detachment. The collapsing
vitreous creates the tear and remains attached
only to the anterior leaflet of retina, thus
allowing free mobility of the posterior flap
(Figure 8.11). This mobile posterior flap of retina
facilitates the entrance of liquefied vitreous into
the subretinal space and can lead to rapidly pro-
gressing detachments, particularly if the tear is
superior in location (Figure 8.12).
Horseshoe tears
Areas of strong vitreoretinal adhesion cause
retinal breaks during traumatic or spontaneous
posterior vitreous detachment. These retinal

Figure 8.12 A posterior vitreous detachment exerts
persistent traction on the posterior lip of torn retina,
frequently leading to rapid influx of fluid into the
subretinal space and a rapidly developing retinal
detachment. Modified from Ryan SJ. Retina, 4th ed.
St Louis: Mosby, 2006.
breaks typically take the shape of a horseshoe.
Detachments related to horseshoe tears have
been reported to account for 11% of traumatic
retinal detachments and 45% of spontaneous
detachments. Furthermore, a history of trauma
was present in 5% and objective evidence of
trauma was found in 20% of detachments associ-
ated with horseshoe tears. As would be expected,
patients with trauma-related horseshoe detach-
ments are younger than those with non-traumatic
detachments. However, assigning a traumatic
etiology to these cases can be difficult.
When vitreous syneresis leads to a posterior
vitreous detachment, horseshoe tears normally
occur at sites of vitreoretinal adhesion. A similar
mechanism occurs in traumatic horseshoe tear
development. Globe deformation and torsion
lead to posterior vitreous detachment, and a tear
can develop at the site of fi rm vitreoretinal adhe-
sion. A flap of retina is held open by residual
Closed globe injuries: posterior segment
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
detected were located near the equator.134
Direct contusive trauma may cause retinal
necrosis and ischemia at the impact site. In one
study, irregular necrotic retinal breaks were
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
vascular damage, and retinal capillary necrosis
contribute to the weakened retina at the impact
site.136 Similar injury following countercoup
trauma has also been reported.137 Such damage
may result in the formation of irregularly shaped
retinal breaks. The most common location of
such breaks is the inferotemporal quadrant, due
to the more exposed position of the globe and
the natural supraduction of the eye with lid
closure (Bell’s phenomenon). Detachments asso-
ciated with necrotic retinal breaks tend to form
quickly, often within 24 hours.
Vitreous base avulsion
Contusive ocular injury may avulse the vitreous
base from its fi rm adhesion straddling the ora
serrata. In fact, vitreous base avulsion is consid-
ered pathognomonic for contusive ocular trauma.
Vitreous base avulsion has been reported in
25.9% of patients with traumatic retinal detach-
119
 Ocular trauma
ment. Vitreous base avulsions have been reported
to occur in roughly half of patients with retinal
detachments secondary to squash ball injuries.138
The trauma associated with vitreous base avul-
sion is often presumed severe considering the
vitreoretinal adhesions are often strongest at the
vitreous base. Because of this inherently strong
vitreoretinal adhesion, avulsion without con-
comitant pars plana tears, retinal dialyses, or
retinal tears is uncommon. Vitreous base avul-
sions appear as a stripe of translucent vitreous
overlying the peripheral retina or ora serrata,
yielding a ‘bucket handle’ appearance. This con-
dition may be asymptomatic and requires no
treatment if found in isolation. However, the
presence of this fi nding should alert the clinician
to perform a careful examination of the pars
plana, ora serrata, and retinal periphery when
the eye becomes stable enough for scleral depres-
sion, as the incidence of retinal tears and dialyses
is very high.
Traumatic posterior vitreous detachment
Traumatic posterior vitreous detachment (PVD)
alone or in combination with vitreous hemor-
rhage is frequently encountered following closed
globe eye injury. Although neither condition
alone causes permanent loss of function, their
presence often heralds more sinister pathology,
particularly of the peripheral retina. Vitreoreti-
nal adhesions are much greater in young patients.
Since trauma occurs much more frequently in
young patients (particularly males), the likeli-
hood of retinal tears in the setting of a traumatic
PVD is very high. Examination of the anterior
retina and pars plana is vital. If it cannot be
performed in the acute setting owing to con-
comitant ocular injury, patient discomfort, or a
poor view due to hemorrhage, ultrasonography
is an excellent tool to determine if any peripheral
tears or detachments are present. Serial exami-
120
nations are important as the vitreous separation
evolves over days to weeks.
Pars plana tears
The non-pigmented pars plana epithelium is the
anterior extension of the neurosensory retina.
Pars plana tears result almost exclusively from
closed globe contusion. The contusive forces place
traction on the anterior border of the vitreous
base, resulting in tear formation. Penetrating
ocular injury, posterior segment surgery, and
atopy are the only other documented causes.139–141
Interestingly, the retinal tears and detachments
associated with atopic dermatitis may be con-
sidered traumatic in origin, given the clinical
nature of the tears and the propensity for vigorous
ocular rubbing seen in this population.
Pars plana tears are uncommon, seven times
less commonly diagnosed than retinal dialysis.
However, it is likely that pars plana tears are
underdiagnosed since they are usually not associ-
ated with retinal detachment and can only be
seen with anterior scleral depression. The pres-
entation and clinical course of retinal detach-
ments associated with pars plana epithelium
tears are similar to those caused by retinal dialy-
sis. The detachments are shallow with smooth
surfaces. They progress slowly over several
months and are generally asymptomatic until
they involve the macula.142 The typical shallow,
slowly progressive nature of these detachments
is due to the absence of a posterior vitreous
detachment and the anterior tear location. The
posterior vitreous base remains attached, provid-
ing a tamponade that limits access of liquefied
vitreous to the subretinal space.
Treatment
Traumatic breaks that lead to rapid retinal
detachment include necrotic retinal breaks,
horseshoe tears, and giant retinal tears. At times,

the vitreous may remain formed in eyes with
traumatic tears, and chorioretinal adhesions may
form that lead to spontaneous hole closure. Such
eyes should be monitored closely for progression
to detachment. Prophylactic laser retinopexy or
trans-scleral cryopexy should be considered in
all patients with traumatic peripheral retinal
breaks in the absence of significant subretinal
fluid. Once a detachment forms, surgical inter-
vention is required. As in repair of non-
traumatic detachments, the overall goal of
surgery is to close all retinal breaks and to relieve
all vitreoretinal traction. Retinal reattachment
may be achieved through pneumatic retinopexy,
scleral buckling, and/or pars plana vitrectomy.
The specific clinical situation and surgeon pref-
erence determine the method of repair.
Giant retinal tears rarely present without con-
current retinal detachment owing to the mobile
posterior retinal flap that allows free entry of
fluid into the subretinal space. Moreover, the
retina may fold upon itself preoperatively or
intraoperatively. These tears often require
advanced vitreoretinal techniques such as
perfluorocarbon stabilization, lensectomy, and
silicone oil tamponade. Despite advances in
vitreoretinal surgery, redetachment rates follow-
ing repair may exceed 10% (Figure 8.13).143
Figure 8.13 A complex, recurrent trauma-related
retinal detachment is visible through the dilated pupil.
Closed globe injuries: posterior segment
Visual acuity outcomes are variable. One large
series reported that nearly 65% had a fi nal visual
acuity of 20/200 or better with a range of 20/20
to no light perception. Concomitant macular
pathology may limit visual acuity following
repair, particularly epiretinal membranes and
macular edema.
Anterior traumatic pathology, such as pars
plana tears and retinal dialyses, may lead to a
slowly developing, asymptomatic retinal detach-
ment. Such breaks should be treated with
cryopexy or laser retinopexy in the acute post-
traumatic period if no significant subretinal fluid
is present. If asymptomatic subretinal fluid is
detected months to years after trauma, assess for
stable chronicity of the break and subretinal
fluid. Signs of chronic subretinal fluid include
retinal atrophy, retinal macrocysts, absence of
rugae, and the presence of demarcation lines. If
a demarcation line has developed, the retinal
break and subretinal fluid may heal spontane-
ously, requiring only close observation. In the
presence of significant subretinal fluid without
demarcation, surgical intervention is indicated.
Detachments associated with pars plana tears
or retinal dialyses may be repaired with good
results by scleral buckling with trans-scleral
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
optimum vision. Furthermore, ocular contusion
with enough force to cause posterior segment
121
 Ocular trauma
damage often causes multiple ocular injuries.
Although each posterior segment injury was dis-
cussed individually, it is important for the clini-
cian to maintain a high level of suspicion for
coexisting systemic, orbital, anterior segment,
and posterior segment injuries.
Manifestations of posterior segment trauma
without retinal breaks (vitreous base avulsion
and commotio retinae) may be carefully observed
with short interval serial examinations in the post-
traumatic period. Examinations should include
scleral depression to the ora serrata once the eye
is stable enough to sustain scleral indentation or
serial ultrasounds if media opacity or patient
discomfort precludes ophthalmoscopic examina-
tion. Once the diagnosis of a retinal break or
detachment is made, vitreoretinal consultation is
indicated.
SUMMARY
1. Contusive ocular injury frequently involves
the posterior segment and has frequent
vision-threatening sequelae.
2. Most posterior segment injuries due to
contusive injury involve the vitreoretinal
interface and its reaction to the inciting
injury.
3. Thorough examination of the peripheral
retina and ora serrata is vital in the post-
traumatic setting. If ophthalmoscopic exam-
ination of the retina is not possible, ultrasound
is a good alternative.
4. Serial evaluations of the retina, whether
ophthalmoscopic or ultrasonographic, are
necessary after contusive ocular injury, as
posterior vitreous detachments evolve over
days to weeks.
5. Although often innocuous when found
peripherally, commotio retinae can lead to
permanent and severe changes of vision if
the macula is involved.
122
6. Vitreous hemorrhage is of particular concern
in young children since amblyopia and pro-
gressive myopia may develop rapidly.
7. Choroidal ruptures require serial monitor-
ing for the appearance of choroidal neovas-
cular membranes.
8. Suprachoroidal hemorrhage indicates severe
ocular trauma and portends a poor visual
prognosis.
9. Sclopetaria is a rare but characteristic mani-
festation of high-velocity missile injury.
10. The type of peripheral break in the retina or
pars plana has significant bearing on the
future behavior of retinal detachments and
their subsequent repair.
11. Retinal detachment is the fi nal common
pathway for disturbances of the vitreoretinal
interface.
REFERENCES
1. Goffstein R, Burton TC. Differentiating traumatic from
nontraumatic retinal detachment. Ophthalmology
1982;89:361–368.
2. Dumas JJ. Retinal detachment following contusion of the
eye. Int Ophthalmol Clin 1967;7(1):19–38.
3. Schepens CL, Marden D. Data on the natural history of
retinal detachment: further characterization of certain
unilateral non-traumatic cases. Am J Ophthalmol
1966;61:213–226.
4. Haimann MH, Burton TC, Brown CK. Epidemiology of retinal
detachment. Arch Ophthalmol 1982;100:289–292.
5. Cox MS, Schepens CL, Freeman HM. Retinal detachment
due to ocular contusion. Arch Ophthalmol 1966;76:678–
685.
6. Dana MR, Werner MS, Viana MAG, Shapiro MJ. Spontaneous
and traumatic vitreous hemorrhage. Ophthalmology
1993;100:1377–1383.
7. Lean JS, Gregor Z. The acute vitreous hemorrhage. Br J
Ophthalmol 1980;64:469–471.
8. Rabinowitz R, Yagev R, Shoham A, Lifshitz T. Comparison
between clinical and ultrasound findings in patients with
vitreous hemorrhage. Eye 2004;18:253–256.
9. Macewen CJ. Eye injuries: a prospective survey of 5671
cases. Br J Ophthalmol 1989;73:888–894.

10. Bellows JG. Observations on 300 cases of ocular war
injuries. Am J Ophthalmol 1947;30:309–323.
11. Eagling EM. Ocular damage after blunt trauma to the eye:
its relationship to the nature of the injury. Br J Ophthalmol
1974;58:126–140.
12. Raman SV, Desai UR, Anderson S, Samuel MA. Visual
prognosis in patients with traumatic choroidal rupture.
Can J Ophthalmol 2004;39:260–266.
13. Wyszynski RE, Grossniklaus HE, Frank KE. Indirect choroidal
rupture secondary to blunt ocular trauma. Retina
1988;8:237–243.
14. Estafanous MFG, Seeley M, Traboulsi EI. Choroidal rupture
associated with forceps delivery. Am J Ophthalmol
2000;129:819–820.
15. Hargrave S, Weakley D, Wilson C. Complications of ocular
paintball injuries in children. J Pediatr Ophthalmol
Strabismus 2000;37:338–343.
16. Weidenthal DT, Schepens CL. Peripheral fundus changes
associated with ocular contusion. Am J Ophthalmol
1966;62:465–477.
17. Aguilar JP, Green WR. Choroidal rupture: a histopathologic
study of 47 cases. Retina 1984;4:269–275.
18. Berlin R. Zur sogenannten commotion retinae. Klin
Monatsbl Augenheilkd 1873;1:42–78.
19. Sipperly JO, Quigley HA, Gass JDM. Traumatic retinopathy
in primates: the explanation of commotio retinae. Arch
Ophthalmol 1978;96:2267–2273.
20. Blight R, Hart JCD. Structural changes in the outer retinal
layers following blunt mechanical non-perforating trauma
to the globe: an experimental study. Br J Ophthalmol
1977;61:573–587.
21. Mansour AM, Green WR, Hogge C. Histopathology of
commotio retinae. Retina 1992;12:24–28.
22. Liem AT, Keunen JEE, Van Norren D. Reversible cone
photoreceptor injury in commotio retinae of the macula.
Retina 1995;15:58–61.
23. Meyer CH, Rodrigues EB, Mennel S. Acute commotio retinae
determined by cross-sectional optical coherence
tomography. European J Ophthalmol 2003;13:816–818.
24. Gregor Z, Ryan SJ. Blood–retinal barrier after blunt trauma to
the eye. Graefes Arch Clin Exp Ophthalmol 1982;219:205–208.
25. Thompson JT, Stoessel KM. An analysis of the effect of
intravitreal blood on visual acuity. Am J Ophthalmol
1987;104:353–357.
26. Butner RW, McPherson AR. Spontaneous vitreous
hemorrhage. Ann Ophthalmol 1982;14:268–270.
27. Lindgren G, Sjodell L, Lindbloom B. A prospective study of
dense spontaneous vitreous hemorrhage. Am J Ophthalmol
1995;119:458–465.
Closed globe injuries: posterior segment
28. Morse PH, Aminlari A, Scheie HG. Spontaneous vitreous
hemorrhage. Arch Ophthalmol 1974;92:297–298.
29. Forrester JV, Lee, WR, Williamson J. The pathology of
vitreous hemorrhage. I. Gross and histological appearances.
Arch Ophthalmol 1978;96:703–710.
30. Regnault FR. Vitreous hemorrhage: an experimental study.
I. A macroscopic and isotopic study of the evolution of
whole blood and hemoglobin. Arch Ophthalmol
1970;83:458–465.
31. Kerman BM, Hreiger AE, Straatsma BR. Resorption of
intravitreal blood following vitrectomy. Am J Ophthalmol
1976;82:915–922.
32. Braendstrup P. Vitreous hemorrhage in the newborn: a rare
type of neonatal intraocular hemorrhage. Acta Ophthalmol
1969;47:502–513.
33. Keenum DG, Boldt HC, Byrne SF. Modern diagnostic
techniques in the evaluation of ocular trauma. Ophthalmol
Clin North Am 1995;8:589–608.
34. Blumenkranz MS, Byrne SF. Standardized echography
(ultrasonography) for the detection and characterization of
retinal detachment. Ophthalmology 1982;89:821–831.
35. DiBernardo C, Blodi B, Byrne SF. Echographic evaluation of
retinal tears in patients with spontaneous vitreous
hemorrhage. Arch Ophthalmol 1992;110:511–514.
36. Vote BJ, Membrey WL, Casswell AG. Vitreous haemorrhage
without obvious cause: national survey of management
practices. Eye 2005;19:770–777.
37. Saxena S, Jalali S, Verma L, Pathengay A. Management of
vitreous hemorrhage. Indian J Ophthalmol 2003;51:189–
196.
38. Sarrafizadeh R, Hassan TS, Ruby AJ, et al. Incidence of retinal
detachment and visual outcome in eyes presenting with
posterior vitreous separation and dense fundus-obscuring
vitreous haemorrhage. Ophthalmology 2001;108:2273–
2278.
39. Ferrone PJ, de Juan Jr. E. Vitreous hemorrhage in infants.
Arch Ophthalmol 1994;112:1185–1189.
40. Mohney BG. Axial myopia associated with dense vitreous
hemorrhage of the neonate. J AAPOS 2002;6:348–353.
41. Miller-Meeks MJ, Bennett SR, Keech RV, Blodi CF. Myopia
induced by vitreous hemorrhage. Am J Ophthalmol
1990;109:199–203.
42. Spraul CW, Grossniklaus HE. Vitreous hemorrhage.
Surv Ophthalmol 1997;42:3–39.
43. Cardillo JA, Stout JT, LaBree L, et al. Post-traumatic
proliferative vitreoretinopathy. Ophthalmology
1997;104:1166–1173.
44. Ryan SJ. Traction retinal detachment. XLIX Edward Jackson
Memorial Lecture. Am J Ophthalmol 1993;115:1–20.
123
 Ocular trauma
45. Kuhn F, Morris R, Mester V, Witherspoon C. Internal limiting
membrane removal for traumatic macular holes.
Ophthalmic Surg Lasers 2001;32:308–315.
46. Yamashita T, Uemara A, Uchino E, Doi N, Ohba N.
Spontaneous closure of traumatic macular hole.
Am J Ophthalmol 2002;133:230–235.
47. Weinstock SJ, Morin JD. Traumatic macular hole.
Can J Ophthalmol 1976;11:249–251.
48. Atmaca LS, Yilmaz M. Changes in the fundus caused
by blunt ocular trauma. Ann Ophthalmol 1993;25:
447–452.
49. Madreperla SA, Benetz BA. Formation of a traumatic
macular hole. Arch Ophthalmol 1997;115:1210–1211.
50. Wainwright D, Fuchshuber P. Delayed spinal cord damage
and a unilateral macular hole following electrical trauma.
Injury 1994;25:275–276.
51. Espaillat A, Janigian RJ, To K. Cataracts, bilateral macular
holes, and rhegmatogenous retinal detachment induced
by lightning. Am J Ophthalmol 1999;127:216–217.
52. Thach AB, Lopez PH, Snady-McCoy LC, Golub BM, Frambach
DA. Accidental Nd : YAG laser injuries to the macula. Am J
Ophthalmol 1995;119:767–773.
53. Sou R, Kusaka S, Ohji M, Gomi F, Ikuno Y, Tano Y. Optical
coherence tomographic evaluation of a surgically treated
traumatic macular hole secondary to Nd : YAG laser injury.
Am J Ophthalmol 2003;135:537–539.
54. Ciulla TA, Topping TM. Surgical treatment of a macular hole
secondary to accidental laser burn. Arch Ophthalmol
1997;115:929–930.
55. Alhalel A, Glovinsky Y, Treister G, Bartov E, Blumenthal M,
Belkin M. Long-term follow up of accidental parafoveal laser
burns. Retina 1993;13:152–154.
56. Aaberg TM. Macular holes: a review. Surv Ophthalmol
1970;15:139–162.
57. Garcia-Arumi J, Corcostegui B, Cavero L, Sararols L. The role
of vitreoretinal surgery in the treatment of posttraumatic
macular hole. Retina 1997;17:372–377.
58. Yanigiya N, Akiba J, Takahashi M, et al. Clinical characteristics
of traumatic macular holes. Jpn J Ophthalmol 1996;40:
544–547.
59. Yamada H, Sakai A, Yamada E, et al. Spontaneous
closure of traumatic macular hole. Am J Ophthalmol
2002;134:340–347.
60. Kusaka S, Fujikado T, Ikeda T, Tano Y. Spontaneous
disappearance of traumatic macular holes in young
patients. Am J Ophthalmol 1997;123:837–839.
61. Mizusawa Y, Ichibe M, Yoshizawa T, Ando N. Clinical
evaluation of traumatic macular hole. Jpn Rev Clin
Ophthalmol 1996;90:790–792.
124
62. Tomii A, Ikeda N, Kurusu A, Mimura O. Clinical curse of
traumatic macular hole. Jpn J Clin Ophthalmol 1999;53:
1274–1278.
63. Nunode S, Nakajuma M, Watanabe C. A case of traumatic
macular hole with interesting course. Jpn Rev Clin
Ophthalmol 1983;77:922–924.
64. Murakami A, Sawa H, Ikeda T, Kawashima A. Two cases of
spontaneous closure to traumatic macular hole. Jpn J Clin
Ophthalmol 1998;52:473–476.
65. Parmar DN, Stanga PE, Reck AC, et al. Imaging of a
traumatic macular hole with spontaneous closure.
Retina 1999;19:470–472.
66. Chow DR, Williams GA, Trese MT, et al. Successful
closure of traumatic macular holes. Retina 1999;19:
405–409.
67. Amari F, Ogino N, Matsumura M, Negi A, Yoshimura N.
Vitreous surgery for traumatic macular hole. Retina
1999;19:410–413.
68. Von Graefe A, Zwei von rutur der choroida. Graefes Arch
Clin Exp Ophthalmol 1854;1:402.
69. Kohno T, Miki T, Shiraki K, Kano K, Hirabayashi-Matsushita M.
Indocyanine green angiographic features of choroidal
rupture and choroidal vascular injury after contusion ocular
injury. Am J Ophthalmol 2000;129:38–46.
70. Godtfredsen E. Re-examination of central ruptures of the
choroid. Acta Ophthalmol 1942;20:337–350.
71. Kaufer G, Zimmerman LE. Direct rupture of the choroid.
Arch Ophthalmol 1966;75: 384–385.
72. Hart JCD, Natsikos VE, Raistrick ER, Doran RML. Indirect
choroidal tears at the posterior pole: a fluorescein
angiographic and perimetric study. Br J Ophthalmol
1980;64:59–67.
73. Secretan M, Sickenberg M, Zografos L, Piguet B.
Morphometric characteristics of traumatic choroidal
ruptures associated with neovascularization. Retina
1998;18:62–66.
74. Fuller B, Gitter KA. Traumatic choroidal rupture with late
serous detachment of macula: report of successful argon
laser treatment. Arch Ophthalmol 1973;89:354–355.
75. Gitter KA, Slusher M, Justice Jr. J. Traumatic hemorrhagic
detachment of retinal pigment epithelium. Arch
Ophthalmol 1968;79:729–732.
76. Gross JG, King LP, de Juan Jr. E, Powers T. Subfoveal
neovascular membrane removal in patients with
traumatic choroidal rupture. Ophthalmology
1996;103:579–585.
77. Wood CM, Richardson J. Indirect choroidal ruptures:
aetiological factors, patterns of ocular damage, and final
visual outcome. Br J Ophthalmol 1990;74: 208–211.

78. Maberly AL, Carvounis EP. The visual field in indirect
traumatic rupture of the choroid. Canadian J Ophthalmol
1977;12:147–154.
79. Gotzaridis EV, Vakalis AN, Sethi CS, Charteris DG. Surgical
removal of sequential epiretinal and subretinal neovascular
membranes in a patient with traumatic choroidal rupture.
Eye 2003;17:790–791.
80. Hilton GF. Late serosanguineous detachment of the macula
after traumatic choroidal rupture. Am J Ophthalmol 1975;79:
997–1000.
81. Leys A, Dralands L, Missotten L. Late complications of
choroidal ruptures. Bull Soc Belge Ophtal 1981;193:
137–141.
82. Smith RE, Kelley JS, Harbin TS. Late macular complications
of choroidal ruptures. Am J Ophthalmol 1974;77:650–658.
83. Dubovy SR, Guyton DL, Green WR. Clinicopathologic
correlation of chorioretinitis sclopetaria. Retina
1997;17:510–520.
84. Arend O, Remky, Elsner AE, Wolf S, Reim M. Indocyanine
green angiography in traumatic choroidal rupture:
clinicoangiographic case reports. German J Ophthalmol
1995;4:257–263.
85. Baltatzis S, Ladas ID, Panagiotidis D, Theodossiadis GP.
Multiple posttraumatic choroidal ruptures obscured by
hemorrhage: imaging with indocyanine green angiography.
Retina 1997;17:352–354.
86. Yilmaz G, Aydin P. Visualization of choroidal rupture with
indocyanine green angiography. Retina 2000;20:315–316.
87. Wood CM, Richardson J. Chorioretinal neovascular
membranes complicating contusional eye injuries with
indirect choroidal ruptures. Br J Ophthalmol 1990;74:93–96.
88. Hart CD, Raistrick R. Indirect choroidal tears and late onset
serosanguinous maculopathies. Graefes Arch Clin Exp
Ophthalmol 1982;218:206–210.
89. Harissi-Dagher M, Sebag M, Gauthier D, Marcil G, Labelle P,
Arbour JD. Photodynamic therapy in young patients with
choroidal neovascularization following traumatic choroidal
rupture. Am J Ophthalmol 2005;139(4):726–728.
90. Mennel S, Hausmann N, Meyer CH, Peter S. Photodynamic
therapy and indocyanine green guided feeder vessel
photocoagulation of choroidal neovascularization
secondary to choroid rupture after blunt trauma. Graefes
Arch Clin Exp Ophthalmol 2005;243(1):68–71.
91. Manschot WA. The pathology of expulsive hemorrhage.
Am J Ophthalmol 1955;40:15–24.
92. Samuels B. Postoperative nonexpulsive subchoroidal
hemorrhage. Arch Ophthalmol 1931;6:840.
93. Winslow RL, Stevenson W, Yanoff M. Spontaneous expulsive
choroidal hemorrhage. Arch Ophthalmol 1974;92: 33–36.
Closed globe injuries: posterior segment
94. Beyer CF, Peyman GA, Hill JM. Expulsive choroidal
hemorrhage in rabbits: a histopathologic study. Arch
Ophthalmol 1989;107:1648–1653.
95. Chu TG, Cano MR, Green RL, Ligget PE, Lean JS. Massive
suprachoroidal hemorrhage with central retinal apposition:
a clinical and echographic study. Arch Ophthalmol
1991;109:1575–1581.
96. Reynolds MG, Haimovici R, Flynn HW, DiBernardo C, Byrne
SF, Feuer W. Suprachoroidal hemorrhage. Ophthalmology
1993;100:460–465.
97. Williams DK, Rentiers PK. Spontaneous expulsive choroidal
hemorrhage. Arch Ophthalmol 1970;83:191–194.
98. Scott IU, Flynn HW Jr, Schiffman J, Smiddy WE, Ehlies F,
Murray TG. Vitreoretinal surgery outcomes among patients
with appositional suprachoroidal hemorrhage.
Ophthalmology 1997;104:2039–2046.
99. Byrne SF, Green RL. Ultrasound of the Eye and Orbit,
2nd edn. St. Louis: Mosby; 1992:104–106.
100. Liggett PE, Mani N, Green RE, Cano M, Ryan SJ, Lean JS.
Management of traumatic rupture of the globe in aphakic
patients. Retina 1990;10:S59–S64.
101. Wirostko WJ, Han DP, Mieler WF, Pulido JS, Connor TB Jr,
Kuhn E. Suprachoroidal hemorrhage: outcome of surgical
management according to hemorrhage severity.
Ophthalmology 1998;105:2271–2275.
102. Gressel MG, Parrish RK II, Heuer DK. Delayed nonexpulsive
suprachoroidal hemorrhage. Arch Ophthalmol 1984;102:
1757–1760.
103. Ruderman JM, Harbin TS Jr, Campbell DG. Postoperative
suprachoroidal hemorrhage following filtration procedures.
Arch Ophthalmol 1986;104:201–205.
104. Lakhanpal V, Schocket SS, Elman MJ, Nirankari VS.
A new modified vitreoretinal surgical approach in the
management of massive suprachoroidal hemorrhage.
Ophthalmology 1989;96:793–800.
105. Welch JC, Spaeth GL, Benson WE. Massive suprachoroidal
hemorrhage: follow-up and outcome of 30 cases.
Ophthalmology 1988;95:1202–1206.
106. Cohn H. Schussverletzungen des Auges. Breslau, Ferdinand
Enke. 1872,24. (As cited in Richards RD, West CE, Meisels AA.
Chorioretinitis sclopetaria. Am J Ophthalmol 1968;66:
852–860.)
107. Goldzieher W. Beitrag zur pathlogie der orbitalen
schussverletzungen. Z Augenh 1902;6:277–281.
108. Sommers IG. Histology and Histopatholgy of the
Eye and its Adnexa. New York: Grune and Stratton;
1949:73.
109. Magulari S, Hartnett E. Radial choroidal ruptures in
sclopetaria. J Am Coll Surg 2003;197:689–690.
125
 Ocular trauma
110. Martin DF, Awh CC, McCuen BW, Jaffe GJ, Slott JH,
Machemer R. Treatment and pathogenesis of traumatic
chorioretinal rupture (sclopetaria). Am J Ophthalmol
1994;117:190–200.
111. Perry HD, Rahn EK. Chorioretinitis sclopetaria. Arch
Ophthalmol 1977;95:328–329.
112. Richards RD, West CE, Meisels AA. Chorioretinitis sclopetaria.
Am J Ophthalmol 1968;66:852–860.
113. Brown GC, Tasman WS, Benson WE. BB-gun injuries to the
eye. Ophthalmic Surg 1985;16:505–508.
114. Cox MS. Retinal breaks caused by blunt non-perforating
trauma at the point of impact. Trans Am Ophthalmol Soc
1980;78:414–466.
115. Otto CS, Nixon KL, Mazzoli RA, et al. Chorioretinitis
sclopetaria from BB ex memoria. Ophthalmic Surg Lasers
2001;32:152–155.
116. Beatty S, Smyth K, Au Eong KG, Lavin MJ. Chorioretinitis
sclopetaria: case report. Injury, Int J Care Injured
2000;31:55–60.
117. Hart JCD, Natsikos VE, Raistrick ER, Doran RML. Chorioretinitis
sclopetaria. Trans Ophthal Soc UK 1980;100:276–281.
118. Katsumata S, Takahashi J, Tamai M. Chorioretinitis
sclopetaria caused by fishing line sinker. Jpn J Ophthalmol
1984;28:69–74.
119. Ross WH. Retinal dialysis: lack of evidence for a genetic
cause. Can J Ophthalmol 1991;26:309–312.
120. Hagler WS. Retinal dialysis: a statistical and genetic study to
determine pathogenic factors. Trans Am Ophthalmol Soc
1980;78:686–733.
121. Lefferstra LJ. Disinsertions of the ora serrata.
Ophthalmologica 1950;119:1–16.
122. Verdaguer TJ, Rojas B, Lechuga M. Genetical studies in
nontraumatic retinal dialysis. Mod Probl Ophthalmol
1975;15:34–39.
123. Zion VM, Burton TC. Retinal dialysis. Arch Ophthalmol
1980;98:1971–1974.
124. Brockhurst RJ. Retinal dialysis. Arch Ophthalmol
1971;85:637–638.
125. Malbran E, Dodds R, Hulbug R. Traumatic retinal
detachment. Mod Probl Ophthalmol 1972;10:479–489.
126. Cameron ME. Non-traumatic dialysis in the young. Br J
Ophthalmol 1960;44:541–546.
126
127. Ross WH. Traumatic retinal dialysis. Arch Ophthalmol
1981;99:1371–1374.
128. Shapland CD. Anterior retinal dialysis. Proc Royal Soc Med
1949;42:609–614.
129. Kennedy CJ, Parker CE, McAllister IL. Retinal detachment
caused by retinal dialysis. Aust NZ J Ophthalmol
1997;25:25–30.
130. Norton EWD, Aaberg TA, Fung W, Curtin VT. Giant retinal
tears. 1. Clinical management with intravitreal air. Am J
Ophthalmol 1969;68:1011–1021.
131. Kanski JJ. Giant retinal tears. Am J Ophthalmol 1975;79:
846–852.
132. Leaver PK, Billington BM. Vitrectomy and fluid/silicone oil
exchange for giant retinal tears: 5 years follow up. Graefes
Arch Clin Exp Ophthalmol 1989;227:323–327.
133. Aylward GW, Cooling RJ, Leaver PK. Trauma-induced retinal
detachment associated with giant retinal tears. Retina
1993;13:136–141.
134. Atmaca LS, Yilmaz M. Changes in the fundus caused by
blunt ocular trauma. Ann Ophthalmol 1993;25:447–452
135. Johnston PB. Traumatic retinal detachment.
Br J Ophthalmol 1991;75:18–21.
136. Duke-Elder S. Concussions and Contusions: System of
Ophthalmology. London: Kimpton, 1972;14:63–310.
137. Longstaff S, Baines PS, Roxburgh STD. Retinal break
formation following countercoup trauma: case report.
Br J Ophthalmol 1987;71:375–376.
138. Knorr HLJ, Jonas JB. Retinal detachments by squash ball
accidents. Am J Ophthalmol 1996;122:260–261.
139. Tasman W. Retinal detachment with breaks in the pars
plana. Br J Ophthalmol 1968;52:181–183.
140. Nakatsu A, Wada Y, Kondo T. Retinal detachment with
atopic dermatitis. Ophthalmologica 1995;209:160–164.
141. Oka C, Ideta H, Nagasaki H, et al. Retinal detachment with
atopic dermatitis similar to traumatic retinal detachment.
Ophthalmology 1994;101:1050–1054.
142. Alappatt JJ, Hutchins RK. Retinal detachments due to
traumatic tears in the pars plana ciliaris. Retina 1998;18:
506–509.
143. Zillis JD, McCuen BW, DeJuan E, et al. Results of silicone oil
removal in advanced proliferative vitreoretinopathy. Am J
Ophthalmol 1989;108:15–21.

Closed globe injuries:
eyelid lacerations
Kambiz K. Parsa, Wendy W. Lee
INTRODUCTION
The approach to any patient with trauma is uni-
versal. The patient must be systematically evalu-
ated and life-threatening injuries, if present,
must be addressed and prioritized before evalu-
ation of the eye and ocular adnexa begins. In this
chapter we will discuss the specifics of evaluat-
ing and treating a patient with an eyelid lacera-
tion. Particular emphasis will be given to history
taking, physical examination, and surgical repair
of the most common types of eyelid lacerations.
More extensive eyelid and orbital injuries are
beyond the scope of this text and require con-
sultation with an oculoplastic specialist.
Depending on the mechanism of injury, the
eyelids may display multiple injury types. These
include:
1. Contusion: superficial impact injury associ-
ated with ecchymoses and soft tissue swelling
(Figure 9.1)
2. Abrasion: scraping, usually an epithelial loss
3. Avulsion: tearing of tissue (Figure 9.2)
4. Puncture: passage of a sharp object through
tissue planes
5. Laceration: cut tissue, typically caused by a
sharp object (Figure 9.3).
The key to any good surgical outcome is a com-
plete understanding of the regional anatomy.
The eyelid is a unique structure that is anatomi-
cally divided into two layers, or lamellae (Figure
9.4A). The anterior and posterior lamellae are
closed separately during full-thickness eyelid
laceration repair. The upper and lower eyelids
have important anatomical differences (Figure
9.4B). The upper eyelid is larger, is supported by
9
a larger tarsal plate, and maintains its position
primarily with the levator aponeurosis. The
lower eyelid is smaller, is supported by a smaller
tarsal plate, and maintains its position primarily
with the lower eyelid retractors. Of particular
interest is the lacrimal drainage system (Figure
9.4C), a system whose structural integrity is
paramount when evaluating and repairing eyelid
lacerations.
EVALUATION
Initial evaluation of the patient begins with a
comprehensive history. Spending focused time
on the history will help guide the physical exam-
ination. At times it may be difficult to obtain a
reliable history from the patient. Patients who
are under the influence of recreational drugs may
not be good historians. Many patients with
extensive injuries may be unresponsive or even
intubated. Children might attempt to conceal
the details of injury for fear of parental punish-
ment. If attempts to obtain a reliable history
from the patient are unsuccessful, try to locate
an eyewitness or family member who may be
able to provide further detail.
Focus should be placed on the timing, mecha-
nism and location of injury. The time an injury
occurred needs to be carefully documented so
the physician can decide if adequate time has
passed for associated edema to subside or
improve. This in turn helps determine the timing
of repair.
Understanding the mechanism and location of
the trauma helps determine the extent and depth
of injury to the tissues and the likelihood of
127
 Ocular trauma
Figure 9.1 Eyelid contusion, typical of assault-related
injuries.
Figure 9.2 Upper eyelid avulsion.
other associated injuries or retained foreign
bodies. If the person was struck with an object,
several questions must be asked:
1. Was the object blunt or sharp?
2. What was the constitution of the object
(organic vs. non-organic)?
3. Was the object embedded in the eyelid and if
so, was it removed? Was the object removed
whole or in pieces?
The answers to these questions further direct
the examination and raise or lower the suspicion
of underlying globe injury. Eyelid injury caused
128
Figure 9.3 Lacerations of the upper and lower eyelids
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
immunization should receive 250 units of human
tetanus immune globulin intramuscularly. If the
patient has not had a tetanus booster in the past
10 years, administer intramuscular or subcuta-
neous tetanus toxoid (0.5 ml).1
A complete ocular exam is indicated in all
trauma patients to assess potential damage to the
globe. After the eye has been fully evaluated (see
Chapter 3), attention can be focused on the
eyelids and ocular adnexa.
Most eyelid injuries can be examined at the slit
lamp without difficulty. However, the discom-
fort associated with extensive eyelid lacerations
usually makes complete inspection difficult
 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,
complete inspection and cleansing of a wound is
typically not feasible without extensive mani-
pulation. The authors prefer to anesthetize
these wounds with a local injection of 2%
lidocaine with epinephrine when the wound
must be manipulated or irrigated. Not only does
this relieve pain, but it provides improved
hemostasis.
Inspection tips
• Anesthetize and cleanse the wound appro-
priately to allow for a more comfortable and
complete examination.
• Gently pull apart the wound, as fibrin may
be holding the wound together and give the
false impression that a laceration is less
extensive.
• Inspect for foreign bodies.
• Inspect the eyelid margin. Evert the eyelid to
look for posterior tarsal lacerations that may
not be associated with anterior lamellar
lacerations.
• Inspect the medial canthus carefully to look
for canalicular injuries. If you suspect a cana-
licular injury, carefully use a 00 Bowman
probe inserted through both the upper and
lower punctum individually. If any portion of
the probe is exposed, a canalicular laceration
is confi rmed. Take care not to create a false
passage.
• When the lacrimal system is injured, suspect
medial canthal tendon injuries. The lacrimal
sac lies between the anterior and posterior
limbs of the medial canthal tendon. Look for
lateral displacement of the medial canthal
angle. If suspicious, consult an oculoplastic
specialist.
• What may appear to be a simple anterior
lamellar laceration may extend into the deep
layers. Look for orbital fat in the wound as a
sign that the septum has been violated, indi-
130
cating deeper orbital injury. Be suspicious of
a levator aponeurosis laceration in this case.
Horizontal upper eyelid lacerations associated
with acute ptosis may also indicate damage to
the levator aponeurosis. However, assessing
the level of ptosis may be difficult due to
severe periorbital swelling. Traumatic ptosis
can occur without a laceration to the levator
muscle or aponeurosis.
• If the patient is conscious and responsive,
attempt to assess levator function by asking
the patient to look up. Horizontal lacerations
of the levator aponeurosis often need repair,
preferably by an oculoplastic specialist.
• Evaluate the degree of eyelid edema and
determine if wound edges can be reapproxi-
mated without tension. Wound tension can
lead to dehiscence and scarring.
Retained orbital foreign bodies are a significant
concern as they can cause a severe inflammatory
reaction or infection. If the possibility of a
foreign body exists, imaging is often employed
to identify and localize the foreign material.
Computed tomography (CT) may confi rm or
reveal retained foreign bodies as well as detect
retrobulbar hemorrhage, a violated globe or
orbital fractures. If the possibility of a retained
metallic foreign body can be eliminated by
history, examination, or plain radiographs, orbital
magnetic resonance imaging (MRI) has higher
resolution and can sometimes detect non-
metallic foreign bodies (e.g. organic material)
more readily than CT.
EYELID LACERATIONS: GENERAL
CONSIDERATIONS
Once an eyelid laceration is identified, a surgical
strategy is formulated. If periorbital swelling
precludes immediate closure, repair can be
delayed several days if necessary. Waiting in such
a case is beneficial because edema may create

undue tension against the newly approximated
wound and may distort the anatomy making
optimal closure of the proper layers difficult.
Postponing closure of an eyelid laceration is pos-
sible because of the extensive vascularity in these
tissues, a unique characteristic of the eyelid and
facial soft tissue.
Ice packs are applied to the wound to decrease
swelling. An antibiotic ointment is used fre-
quently to prevent infection and maintain lubri-
cation of the wound. Management of an eyelid
laceration is undertaken after the management
of any globe injury.2 If the globe is ruptured or
lacerated, repair of the eyelid laceration is typi-
cally deferred to prevent undue pressure on the
wounded globe. If the eyelid laceration is not
edematous and the wound can be reapproxi-
mated without tension, it can be repaired during
the same visit to the operating room but after
globe repair.
General anesthesia is recommended for most
children because they may not tolerate probing
of the injured tissue or local injection of
anesthetic. Older children and adult patients
with significant anxiety can benefit from local
anesthetic with sedation (often an oral ben-
zodiazepine). However, most adult patients
can tolerate local anesthesia without sedation.
We routinely use lidocaine 2% with epinephrine
to allow anesthesia with vasoconstriction.
Epinephrine should be avoided in patients
with uncontrolled hypertension or cardiac
arrhythmias.
When planning repair of eyelid lacerations,
general principles to take into consideration
include:
• Assemble a surgical team that is familiar with
ophthalmic instruments.
• Protect the globe. Plastic or metal protective
covers are commercially available and are
placed on the eye before the eyelid repair to
prevent inadvertent needle penetration.
Closed globe injuries: eyelid lacerations
• Anesthetize the tissues prior to cleansing and
inspecting as outlined previously.
• Sterilize the surgical field with povidone
iodine or an appropriate alternative if the
patient has an allergy to topical iodine.
• Isolate the wound with sterile drapes.
• Inspect for foreign bodies and irrigate copiously.
• Pull lacerated tissues apart during inspection,
as fibrin tends to hold lacerated edges together,
causing underestimation of the actual extent
of the laceration.
• Inspect for tissue loss, although this is an
unusual circumstance. Most of the time soft
tissue edema and retraction of the tissues
contribute to a false appearance of tissue loss.
Once the edema subsides and the deeper
tissues are reapproximated, superficial tissues
tend to fall into place and the cut edges of the
skin fit together like pieces of a puzzle.
• Preserve and restore eyelid anatomy and
function.
NON-MARGINAL EYELID LACERATIONS
Inspection, as described above, is vital when
approaching eyelid lacerations. Gently pulling
tissues apart and probing their extent is vital to
properly close all layers and prevent retention of
foreign bodies. Depth of injury is particularly
vital. If preaponeurotic fat is encountered, this
indicates that the orbital septum has been vio-
lated. If the upper lid is involved, the wound is
inspected for a laceration of the levator aponeu-
rosis. If the levator aponeurosis is injured and the
patient has blepharoptosis, an oculoplastic spe-
cialist should be consulted for defi nitive repair.
Vertical aponeurotic tears usually heal without
treatment and do not require suture repair.
Subcutaneous closure
An absorbable suture such as 5-0 polyglactic acid
(Vicryl®, Ethicon, Somerville, NJ) on a spatu-
131
 Ocular trauma
lated needle is our choice for deep tissue closure
in the periocular region. This suture can be used
for deep tissue closure above the brow. It can also
be used to anchor deep tissues to the periosteum
to take tension off the wound. There is no need to
place deep tissue sutures through the orbicularis
muscle beneath the brow unless required to
diminish tension on the skin sutures. It is also
unnecessary to suture the cut edges of the orbital
septum, as they will heal without treatment.
Most anterior lamellar defects can be closed
primarily. If there is tissue loss, an oculoplastic
specialist should be consulted since advanced
techniques such as skin grafts or flaps may be
necessary to appropriately close the defect.
Skin closure
For most skin closures, the authors prefer 7-0
nylon on a cutting needle below the brow and
6-0 nylon above the brow. The nylon suture is
preferred for skin closure because it creates the
least amount of inflammation and scarring and
it glides easily through the tissues. The suture is
typically removed in 1 week. Absorbable suture
(e.g. 7-0 polyglactic acid) is advisable if follow-
up for suture removal cannot be assured or if
suture removal might not be possible without
anesthesia (e.g. in children).
MARGINAL EYELID LACERATIONS
Primary closure, if possible, is the ideal proce-
dure for repairing a marginal laceration. For
eyelid defects under tension or in cases with
loss of tissue, oculoplastic consultation is typi-
cally necessary. When repairing marginal eyelid
lacerations, similar goals are present for each
case:
1. Realign the eyelid margin.
2. Restore structural integrity of the tarsus.
3. Avoid eyelid notching.
4. Minimize skin and deep tissue scarring.
132
5. Protect the eye. Sutures through the tarsal
plate should be lamellar, especially overlying
the cornea, in order to prevent inadvertent
abrasions or penetrations.
Surgical repair
• Clean, anesthetize, and inspect the eyelid
wound (Figure 9.5A).
• Freshen the lacerated edges and separate the
anterior lamella from the posterior lamella
using blunt dissection. Expose approximately
3 mm of tarsal plate on both sides of the
wound.
• Approximate the tarsus by passing 5-0 poly-
glactic acid sutures on a spatula needle through
partial thickness of the tarsal plate horizon-
tally. Pass each suture approximately 2 mm
from the lacerated edge and exit mid-depth
through the thickness of the tarsal plate. To
prevent corneal or conjunctival abrasions,
evert the eyelid after each pass to make certain
sutures are not exposed on the posterior
surface. Do not tie the knots until all sutures
are in place, as this will make placement of
further sutures difficult. You may need as
many as two or three sutures passed in
similar fashion to properly realign the tarsus
(Figure 9.5B). Leave the sutures untied and
direct attention to reapproximation of the
eyelid.
• Pass a 5-0 silk suture at the level of the mei-
bomian glands in a vertical mattress fashion.
This has been described as the ‘far-far-near-
near’ technique (Figure 9.5C). Take the fi rst
pass about 3–4 mm from the lacerated edge
and exit in the same position on the other side
of the wound. Begin the second pass on the
same side the fi rst pass exited, and pass the
suture approximately 1 mm from the lacera-
tion on both sides.
• Tie the 5-0 polyglactic acid sutures to approx-
imate the tarsal plate (Figure 9.5D).
 Closed globe injuries: eyelid lacerations

A B

C D

Figure 9.5 (A–E) Marginal lid laceration repair.

• Tie the silk mattress suture so the cut edges
slightly pucker. This will ensure good reap-
proximation and prevent lid notching. Leave
the tails of the silk suture long and incorpo-
rate them into the skin sutures to prevent the
knot from rubbing against the cornea.
• Finally, close the overlying skin with inter-
rupted 7-0 nylon or vicryl sutures. Incorpo-
rate the tag ends of the 5-0 silk to keep its
knot away from the cornea (Figure 9.5E).

133
 Ocular trauma
CANALICULAR LACERATIONS
Any laceration in the region of the medial canthus
should be carefully inspected for the possibility
of a canalicular violation. If unsure whether the
canaliculus is involved, the lacrimal punctum
should be dilated and probed with a 0 or 00
Bowman probe, taking care to avoid the creation
of a false passage. If the probe passes through the
system without any areas of exposure, the lacri-
mal drainage system is most likely intact.
Surgical repair
Multiple options are available to repair canalicu-
lar lacerations. These include the use of a mono-
canalicular stent, a bicanalicular donut stent, or
a bicanalicular Crawford stent. The stent allows
proper realignment of the lacerated canalicular
edges and is usually left in place as long as 3–6
months. In the office setting, a Crawford stent is
usually avoided as sedation is typically necessary.
A monocanalicular stent requires canulation of
only one canaliculus. This is particularly helpful
in the small percentage of people who do not
have a common canaliculus, a situation that
renders placement of a donut stent difficult.
Bicanalicular stents such as the Crawford stent
and the donut stent are more stable and are less
likely to become dislodged prior to the intended
removal and are the authors’ preferred method
of repair.
For any method, the surgical site is cleaned,
anesthetized, and draped. Attention is initially
directed at identifying the cut ends of the
canaliculus, fi rst inspecting the tissues with
surgical loupes or an operating microscope.
The white sheen of the epithelial lined tube can
often be readily seen. If this is unsuccessful,
several ‘tricks’ are available to identify the cut
ends:
1. Paint the area with a sterile fluorescein strip
to help visualize the cut ends.
134
2. Inject dyed saline or viscoelastic through the
intact system and watch for passage of fluid
through the lacerated end.
3. Inject air through the punctum and watch for
bubbles at the lacerated edge.
4. If the proximal cut end of the canaliculus is
still not apparent, insert a pigtail probe dipped
in a steroid/antibiotic ointment through the
intact punctum and gently curve it around
toward the injured canaliculus, following the
normal anatomy. Look for the end of the
probe exiting the cut end of the canaliculus.
Care should be taken not to force the pigtail
probe and create a false passage.
Once the cut ends are identified, repair pro-
ceeds. We will discuss each procedure
individually.
Monocanalicular stent
A monocanalicular stent (Mini Monoka; FCI
Ophthalmics Marshfield Hills, MA) can be used
for lacerations involving the external 2/3 of one
canaliculus.
• Identify the lacerated ends of the canaliculus
as outlined above (Figure 9.6A).
• Trim the monocanalicular stent to the appro-
priate size so that the end of the stent rests in
the lacrimal sac (approximately 12 mm).
• Dilate the punctum and advance the stent
through both lacerated edges (Figure 9.6B).
• Approximate the deep soft tissues with inter-
rupted 7-0 polyglactic acid sutures. Pass the
sutures adjacent to the cut ends of the cana-
liculus for best approximation. If tension
needs to be taken off of the wound, use 5-0
polyglactic acid.
• Close the overlying skin with interrupted 7-0
polyglactic acid or nylon sutures.
• Place two interrupted 8-0 vicryl sutures
through both the medial and lateral ends of
the stent footplate to fi xate the stent to the
lid margin (Figure 9.6C).
 Closed globe injuries: eyelid lacerations

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-
licular stent within the canalicular system utiliz-
ing a pigtail probe. The use of the pigtail probe
has been described previously not only for cana-
licular lacerations but also for use in Moh’s
medial canthal reconstructions involving the
lacrimal system. 3
• Pass the pigtail probe through the intact cana-
licular system and exit through the proximal
cut end.
• Thread a 6-0 prolene suture (needle removed)
through the islet of the probe (Figure 9.7A).
Back the probe out, pulling the suture through
the canaliculus.
through the opposite punctum and exit
through the distal cut end. Thread the other
end of the 6-0 prolene into the islet and back
the probe out, pulling the suture through the
punctum. The 6-0 prolene acts as a guide over
which a silicone stent is placed.
• Using a piece of Crawford silicone stent
(remove the internal suture if present), thread
the stent around the 6-0 prolene suture and
through the canalicular system. (Figure 9.7B)
Coating the stent with an antibiotic ointment
may help slide the stent into position. Take
care not to bend the suture as kinks make the
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
edges and out of the opposite punctum.
• Grasp both ends of the silicone stent with a
straight needle holder to prevent the suture or
stent from slipping out of the system.
• Once the canalicular system is fully cannu-
lated with the stent and suture, direct your
attention to reapproximation of the surround-
ing soft tissues as described above. Taking this
step prior to tying the stent will prevent
unnecessarily long stents that may rub against
the cornea.
• After soft tissue closure, adjust the appropri-
ate length of the stent by grasping the ends
with a straight needle holder. The silicone
stent is trimmed to the appropriate length by
removing the excess silicone tubing with a
silicone stripper. The silicone stripper allows

136

the surgeon to score and separate the silicone
tubing without cutting the underlying prolene
suture. Grasp the stripper with your index
fi nger and thumb over the most inferior holes
of the instrument for better dexterity and
control of the instrument. Pinch the instru-
ment around the tubing and gently pull
upwards (Figure 9.7C).
• Once the stent is trimmed to the appropriate
length, tie the prolene suture within the stent
with three knots.
• Rotate the knot into the lacrimal sac gently
using the forceps and needle holders (Figure
9.7D).
Crawford stent
A Crawford stent is typically placed under local
sedation.
• Identify lacerated ends of the injured canalic-
ulus as outlined above.
• Dilate the punctum and advance the stent
into the punctum vertically for approximately
2 mm and then horizontally through the
proximal end of the lacerated canaliculus.
• Carefully cannulate the distal end of the
lacerated canaliculus with the stent.
• Advance the stent until a hard stop is encoun-
tered (Figure 9.8A).
• Redirect the stent vertically and advance
through the nasolacrimal duct. Use a large
Bowman probe inserted underneath the infe-
rior turbinate to ensure the placement of the
probe through the lacrimal drainage pathway
is correct. If the space underneath the inferior
turbinate is limited, the turbinate can be infra-
ctured with a Freer periosteal elevator.
• Retrieve the stent underneath the inferior
turbinate with a groove director such as the
Tse-Anderson Groove director (IOWA) or a
Crawford hook.
• Place the other end of the Crawford stent
through the uninjured punctum, through the
Closed globe injuries: eyelid lacerations
canaliculus and down through the nasolacri-
mal duct in the same manner.
• Retrieve the stent underneath the inferior tur-
binate to complete the intubation of the cana-
licular system (Figure 9.8B).
• Reapproximate the soft tissues surrounding
the canalicular laceration as described previ-
ously. As stated previously, deep vicryl sutures
should be placed as close to the cut ends of
the canalicular epithelium as possible for the
best approximation of the tissues (Figure
9.8C).
• Grasp the stent with straight needle holders
at the entrance of the nostril and strip away
the excess tubing with a stripper as described
above. This excess tubing can be sterilized
and saved for repair of canalicular lacerations
using donut stents as previously described.
• Tie the suture within the lumen of the Craw-
ford stents to itself.
• Anchor the Crawford stent to the nasal vesti-
bule using a 6-0 nylon or prolene suture
passed through the loop of the stent and then
through the lateral tissues just inside the nares
(Figure 9.8D). This suture will prevent the
stent from prolapsing through the puncta and
will make future removal of the stent easier
since the ends can not retract into the naso-
lacrimal duct.
POSTOPERATIVE WOUND CARE
The newly repaired eyelid should be kept clean
and dry. Postoperative edema is diminished by
elevating the patient’s head to 30 degrees and
applying ice packs for the fi rst 48 hours following
surgery.
Pressure patching for up to 1 week, especially
after full-thickness laceration repairs, may be
necessary to immobilize the lid and prevent
undue tension on the newly approximated
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
globe repair, or in monocular patients dependent
on the eye for activities of daily living.
Antibiotic ointment such as ophthalmic baci-
tracin or erythromycin should be applied three
times daily for 1 week. A combination antibi-
otic–steroid ointment is typically used with
canalicular lacerations to lessen scarring. The
patient should be instructed to return if any
unexpected swelling, pain, or secretions develop.
Follow-up is scheduled for 5–7 days, at which
time permanent skin sutures are removed. Eyelid
margin sutures should be left in place for 2
weeks. Stents are left in place for 3–6 months.
Early removal may be necessary if cheese-wiring,
infection, or granuloma develop.
SUMMARY
1. Familiarity of eyelid anatomy is essential
prior to eyelid laceration repair.
2. Thorough cleansing and inspection of an
eyelid laceration often requires injection of
local anesthesia.
3. Lacerated tissues must be separated to deter-
mine the full extent of the injury, since
fibrin can sometimes hold tissues together
giving the false impression of a more super-
ficial injury.
4. Thorough inspection for retained foreign
bodies and copious irrigation with a sterile
solution is utilized for all eyelid lacerations
prior to repair.
Closed globe injuries: eyelid lacerations
5. Proper antibiotic coverage and immunizations
should be given preoperatively if necessary.
6. If orbital fat is apparent in an eyelid wound,
the orbital septum may be violated, and sus-
picion for a laceration of the levator aponeu-
rosis is heightened.
7. If there is any question regarding the struc-
tural integrity of the canalicular system,
each canaliculus should be probed individu-
ally with a small caliber Bowman probe.
8. Repair of eyelid lacerations can be delayed
for 24–48 hours if necessary because of the
extensive vascularity of the involved tissues.
If delayed, have the patient apply ice packs
and an antibiotic ointment to the wound
several times a day.
9. Multiple methods are available to repair
canalicular injuries, the choice of which
depends on both the type of injury and
surgeon experience and preference.
10. Proper alignment of tissues with minimal
tension on the wounds is the key to a suc-
cessful eyelid laceration repair.
REFERENCES
1. Centers for Disease Control. Diphtheria, tetanus, and
pertussis: recommendations for vaccine use and other
preventive measures: recommendations of the Immunization
Practices Advisory Committee (ACIP). MMWR 1991;40
(No. RR-10):1–28.
2. Mindlin AM. Prioritizing the repair of adnexal trauma.
Adv Ophthalmic Plast Reconstr Surg 1987;6:91–101.
3. Jordan DR, Nerad JA Tse DT. The pigtail probe revisited.
Ophthalmology 1990;97:512–519.
139

Closed globe injuries:
orbital trauma
Vivian Schiedler, Thomas E. Johnson, Kenneth B. Krantz
INTRODUCTION
The orbit is the protector of the eye. Its unique
pyramidal shape and thick bony walls serve to
protect the orbital contents (Figure 10.1). Orbital
injuries can occur alone or in combination with
ocular trauma. In most cases, the treatment of
ocular trauma takes precedence over orbital and
periocular injuries. Except for a few visually-
threatening orbital emergencies which require
immediate intervention to prevent permanent
visual loss, the treatment of most traumatic
orbital injuries can be postponed until after the
eye has been stabilized. In cases involving serious
neurologic injury or airway compromise, the
ophthalmologist must take the patient’s global
medical status into consideration when prioritiz-
ing examination and treatment.
In this chapter we will discuss the examination
techniques, diagnosis, and treatment strategies
of the most common orbital injuries.
EPIDEMIOLOGY
Orbital trauma is reported to occur in multiple
situations. Motor vehicle accidents, altercations
with punches to the eye, falls, and sport injuries
involving impact with a ball are some of the
most common causes of trauma to the orbit.
Young males typically account for the majority
of patients presenting with orbital trauma.
When due to motor vehicle accidents, orbital
trauma is typically more severe in unrestrained
passengers.
10
PATHOPHYSIOLOGY
Orbital injury can be classified into contusive or
penetrating injuries, although significant overlap
exists between the two. Objects that transmit a
force to the eye and orbit without entering the
structures cause contusive injuries. These objects
are typically larger than the size of the orbit, for
example fi sts, balls, baseball bats, bottles, and
flat surfaces such as dashboards or doors. Even
without direct tissue penetration by the object,
orbital walls can be fractured and the globe can
be ruptured. Objects that pass through the
orbital or ocular tissues cause penetrating inju-
ries. These objects often have sharp or pointed
edges, but dull or rounded objects can cause
penetration if sufficient velocity is present.
Penetrating objects are often, though not always,
smaller than the orbit in at least one dimension
and include knives, pencils, twigs, bullets,
umbrella tips, and nails. Injury is determined by
the structures that lie in the path of the pene-
trating object.
When evaluating the extent of injury, it is
important to note both the mass and velocity of
the object responsible for orbital trauma. The
velocity of the object is more important than
its size since the energy causing tissue disruption
is determined more by the velocity than by
the mass of a projectile (kinetic energy = 1/2
mass × velocity2).1 Therefore, assuming similar
mass, high velocity objects have more kinetic
energy and subsequently cause more tissue
damage.
141
 Ocular trauma
Sphenoid bone
(lesser wing)
Frontal bone
Sphenoid bone
(greater wing) Ethmoid bone
Zygomatic bone Lacrimal bone
Maxillary bone
Palatine bone
Figure 10.1 The orbital floor is composed of the
maxillary, zygomatic, and palatine bones, and is 0.5–
1 mm thick. The infraorbital neurovascular bundle
travels along the middle of the floor, and most
fractures occur in the thin bone medial to the nerve.
The medial wall is composed of the maxillary, lacrimal,
ethmoid, and lesser wing of sphenoid bones. The
ethmoid bone is very thin (0.2–0.4 mm), and is known
as the lamina papyracea. Most medial wall fractures
occur within the ethmoid bone. The frontoethmoid
suture delineates the location of the cribriform plate.
The maxillary sinus lies beneath the floor, and the
ethmoid sinus lies medial to the medial wall.
EVALUATION
Very rarely do patients present to an ophthal-
mologist with life-threatening injuries. Occa-
sionally patients experiencing sudden visual loss
in association with head or neck trauma may
ignore their more serious injuries and seek oph-
thalmic care fi rst. It may become the ophthal-
mologist’s responsibility to do a general physical
examination to exclude the possibility of life-
threatening, non-ocular conditions, such as
subdural hemorrhage. If injuries are limited to
the eye and ocular adnexae, ocular emergencies
(ruptured globe, intraocular foreign body, central
retinal artery occlusion) should be addressed
fi rst.
142
The importance of a careful history cannot be
overemphasized, as serious orbital injuries may
externally appear trivial. Symptoms such as
decreased vision and diplopia should be specifi-
cally elicited. The timing and mechanism of
injury should be specified. A past medical and
surgical history should be taken. Possible surgi-
cal intervention should be anticipated, so it is
helpful to know the timing of the injury and the
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.
Use of anticoagulants is particularly important
as it may explain relatively minor injuries with
an unexpected amount of associated hemorrhage
and help prepare the surgeon for possible intra-
operative complications.
If available, visual acuity should be checked
with a standard Snellen chart. Spectacle or
pinhole correction should be used to obtain an
accurate result. In the emergency setting, near
visual acuity using a near card will suffice.
If the patient is unconscious, visual acuity
should be documented as soon as the patient
recovers the ability to cooperate with visual
testing.
Many traumatized patients have neurologic
deficits that impair vision testing, making the
pupillary examination paramount. A relative
afferent pupillary defect in the absence of
explanatory eye fi ndings should alert the exam-
iner to the possibility of orbital injuries compro-
mising optic nerve function.
Intraocular pressure is a vital test after orbital
trauma. When orbital trauma leads to changes
in intraocular pressure, it is typically elevated.
Mild transient elevations in intraocular pressure
are seen with many cases of mild orbital edema.
Significantly elevated intraocular pressure in the
absence of intraocular fi ndings should raise sus-
picion of orbital causes. Orbital hemorrhage or
 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
Contusive orbital trauma is usually caused by
fi sts, motor vehicle accidents, and small sports
ball projectiles, including tennis balls, racquet-
balls, and baseballs. The term ‘blowout fracture’
refers to the expansion of orbital volume due to
the fracture of the thin orbital walls into the
adjacent paranasal sinuses. The quality of these
thin bones is actually a protective mechanism,
fracturing to lessen pressure on the globe and
potentially prevent rupture of the eyewall.
There are two main theories regarding the
mechanism of blowout fractures. The ‘hydraulic
theory’ suggests that there is an increase in
orbital hydrostatic pressure transmitted from
direct pressure on the globe, allowing the thin
bony walls to fracture before globe rupture
occurs.4 The ‘buckling theory’ suggests that
pressure directed against the sturdy orbital rim
causes a transient deformation of the bones with
resultant fracture of the thin orbital walls.5,6
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:
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
enophthalmos
6. slit lamp examination for subconjunctival
hemorrhage, conjunctival chemosis and
further ocular injury.
Closed globe injuries: orbital trauma
Subcutaneous emphysema is the accumulation
of air beneath the skin due to a trauma-induced
communication between the paranasal sinuses
and the orbit. One can often feel and hear a
crackling sensation when palpating the perior-
bital tissues in this situation. Subcutaneous
emphysema is often accentuated after the patient
blows his or her nose, forcing air into the tissues
(Figure 10.4). The inferior rectus muscle or its
surrounding fibrous tissues are often entrapped
within the fractured bones of the orbital floor
resulting in restriction of ocular motility on
upgaze (Figure 10.5) and resultant diplopia. This
muscle can also be swollen and hemorrhagic,
resulting in decreased infraduction. One should
test sensation in the infraorbital nerve distribu-
tion, testing sensitivity of the cheek, side of nose,
and teeth on the affected side. Gentle palpation
A
B
Figure 10.4 A patient with an orbital blowout fracture
was evaluated initially (A) and given appropriate
instructions and follow-up. Several days later, he
presented with massive subcutaneous emphysema (B)
and palpable crepitus after forgetting his instructions
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

Figure 10.7 Severe enophthalmos of the right eye
following a large blowout fracture. Note the
subsequent change in the upper eyelid sulcus and the
downward displacement of the eye.
3. injuries that are high risk for future
enophthalmos
a. large fractures of the floor and/or medial
wall
b. combined medial wall and floor fractures.
If diplopia is persistent after 7–10 days, forced
ductions are performed to verify muscle entrap-
ment. Anesthesia is applied to the limbus
inferiorly, using topical lidocaine or tetracaine.
The conjunctiva is grasped with forceps, and the
globe is elevated. A positive test is one in which
the eye is not able to be elevated, indicating
entrapment of the inferior rectus, inferior
oblique, or the fibrous tissue surrounding these
muscles. A forced generation test can also be
performed to determine if muscle dysfunction is
due to swelling or hematoma within the muscle.
Again, the limbus is grasped with a forceps, and
the patient is asked to look in the direction of
action of the muscle in question (typically down
when the inferior rectus is the involved muscle).
The examiner can then determine if any muscle
action is initiated.
It is much easier to correct enophthalmos early,
as late enophthalmos is often complicated by
orbital fat atrophy and shortening of the extra-
ocular muscles. Surgical repair is accomplished
Closed globe injuries: orbital trauma
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
sheets (Supramid), porous polyethylene, Teflon,
bone, and others. The goal is to reconstruct the
normal contour of the orbital walls and reposit
the orbital tissues back into the orbital space.
Care is taken to avoid injury to the infraorbital
nerve that is easily seen running along the orbital
floor. The medial wall can be approached through
the floor incision or through a transcaruncular
incision. A medial wall implant is often neces-
sary if a large fracture is evident in this area.
Small medial wall fractures usually do not need
repair and rarely cause extraocular muscle
entrapment. The periosteum is closed, as well as
the conjunctiva or skin. A silk traction suture
may be left in the lower lid margin and taped to
the forehead during the fi rst postoperative week.
This helps prevent lower lid retraction and offers
corneal protection during the immediate postop-
erative period. Again patients are instructed not
to forcefully blow their nose, and not to engage
in strenuous exercise requiring straining.
Some orbital fractures require urgent surgical
intervention, and cannot wait the usual 7–10
days for edema and hemorrhage to subside. These
are the ‘trapdoor fractures,’ also described as the
‘white-eyed’ blowout fractures.13 This subtype
usually occurs in children and young adults sus-
taining an inferior wall break. This clinical sce-
nario is important to remember since emergent
consultation with an oculoplastic specialist may
be required. A hinged, non-comminuted floor
147
 Ocular trauma
A recommended to identify heart block if symp-
B
Figure 10.8 (A) Surgeon’s view of orbital floor fracture
repair. An orbital implant has been placed to bridge the
gap created by the floor defect. (B) Surgeon’s view at
the end of the case showing the small subciliary
incision utilized during orbital floor fracture repair.
fracture causes a tight entrapment of the inferior
rectus or its perimuscular connective tissue. This
fracture is thought to be similar to a ‘greenstick
fracture’ in which the bones do not break com-
pletely, but fracture, bend, and quickly spring
back into an almost normal configuration due to
the increased elasticity of the bones in younger
individuals.14,15 The temporary deformity of the
floor allows the orbital tissue to become tightly
incarcerated. These patients demonstrate marked
restriction on upgaze. Additionally, they can
present with an oculocardiac reflex with nausea,
vomiting, bradycardia and heart block. This con-
dition can be life-threatening, and an ECG is
148
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
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
enophthalmos. Complications of medial frac-
tures include medial rectus entrapment, orbital
emphysema, a pseudo-Duane’s syndrome in
which the globe retracts and the fi ssure narrows
on attempted abduction, and late enophthal-
mos.17 If a medial wall fracture is large, or if
medial rectus entrapment occurs, surgical inter-
vention is needed.18
Orbital roof fractures can occur with signifi-
cant trauma, usually after motor vehicle acci-
dents or falls from heights (Figure 10.9). These
fractures can involve the frontal sinus and intra-
cranial structures. Complications include CSF
leak due to dural tears, intracranial hemorrhage,
ocular muscle imbalance with painful limitation
of upgaze, ptosis, traumatic encephalocele,
meningitis and brain abscess.19 A superior sub-
periosteal hematoma can result in downward
displacement of the eye. Simple fractures of the
roof without inner table skull fracture can be

Figure 10.9 Large, displaced orbital roof fracture with
traumatic encephalocele formation in the superior
orbit.
repaired through a brow incision. More compli-
cated fracture requires neurosurgical and/or
otorhinolaryngologic consultation.20
Nasoethmoidal fractures result from contusive
trauma to the mid-section of the upper face. The
nasal bones as well as the thin ethmoidal bones
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-
matic telecanthus or nasolacrimal duct obstruction
can be performed by an oculoplastic specialist.
Closed globe injuries: orbital trauma
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
entrapment of orbital contents and diplopia.
Patients often complain of difficulty chewing
(trismus) due to disruption of the temporoman-
dibular joint. Most surgeons recommend early
intervention in tripod fractures, as late repair is
difficult due to fibrosis of the tissues, and may
necessitate osteotomies.
Midfacial fractures are divided into the Le Fort
fractures. Le Fort I fractures involve the lower
Figure 10.10 Flattening of the malar eminence and
rounding of the lateral canthal angle associated with a
tripod fracture.
149
 Ocular trauma
aspect of the maxilla, and do not involve the
orbit. Le Fort II fractures, also called pyramidal
fractures, involve the maxilla, nasal bones, infe-
rior orbital rims, medial orbital walls and floors,
and lacrimal drainage systems. A Le Fort III
fracture, also known as craniofacial dysjunction,
involves the nasal bones, medial and lateral
orbital walls, and zygomatic arches, with the
facial skeleton connected to the cranium only
with soft tissue. Orbital involvement in types II
and III can result in extraocular muscle entrap-
ment and diplopia.
Early postoperative complications of floor and
medial wall fracture repair include infection,
bleeding, loss of vision, and diplopia. If the
orbital implant is too large, optic nerve compres-
sion at the orbital apex can occur. Patients with
an entrapped muscle often have transient post-
operative diplopia due to hemorrhage and edema
within the muscle. Patients with older fractures
can have scarring and fibrosis of the inferior
rectus, and even with complete release may con-
tinue to be diplopic. Strabismus surgery may be
needed to re-establish single vision in this group
of patients. Adequate time after surgery, usually
6 months, is needed to allow postoperative
recovery of muscle function before strabismus
surgery is contemplated.
Late complications are usually related to the
orbital implant. They include infection, migra-
tion, and extrusion.22 Additionally, intraorbital
inclusion cyst can occur, especially if sinus
mucosa remains in the orbit after wall repair.
Rarely, a late bleed into the capsule surrounding
the implant occurs, and patients report pain,
a pressure sensation, inflammation, and
proptosis.23
Repair of old fractures is more difficult, as
they are usually complicated by fibrosis of the
entrapped tissues as well as fat atrophy. However,
good results can often be obtained. Other surgi-
cal options include strabismus surgery to restore
150
single binocular vision in primary position, and
blepharoplasty of the opposite upper eyelid to
mask the enophthalmos of the traumatized
side.7,8
INTRAORBITAL FOREIGN BODIES
Introduction
The majority of intraorbital foreign bodies are a
result of assault, industrial accidents, or freak
accidents at home, at work, or during recreational
activities (Figure 10.11).24 Both sharp and blunt
instruments have been responsible for vision loss
and even death from intracranial extension.
Examples include knives, scissors, pencils,
bullets, BB pellets, fi shhooks, umbrellas, and
twigs, to name but a few.
An intraorbital foreign body should be sus-
pected in patients with a remote or recent history
of trauma, no matter how trivial. Patients may
not recall a specific traumatic event. They may
not seek medical care for small lacerations or
puncture wounds until acute inflammation from
a retained foreign body arises. A high index of
suspicion is especially important in evaluating
children with periocular inflammation. Signs
and symptoms of retained intraorbital foreign
bodies include:25–28
1. orbital mass
2. proptosis
3. painful or restricted eye movements
4. gaze-evoked amaurosis
5. diplopia
6. ptosis
7. lagophthalmos
8. draining sinus tract
9. orbital cellulitis.
Pathophysiology
The size, site, and mechanism of entry as well as
the velocity and composition of the foreign body

A bismus, while damage to the angular artery or
B extraocular muscles, optic nerve, and surround-
Figure 10.11 ‘Freak’ accidents account for a large
percentage of intraorbital foreign bodies. A 27-year-old
male was at work when he was inadvertently injured
with a nail gun (A). The nail is seen entering in the
brow line. A plain X-ray shows the depth of the nail into
the orbit (B). Unfortunately, the nail had entered the
eye, creating a globe laceration and extensive retinal
detachment. Despite repair, vision remained hand
motions.
often determine symptomatology. As would be
expected, large foreign bodies are more likely to
cause more extensive tissue destruction than
smaller ones. However, the location of injury also
matters. Objects penetrating the superior orbit
are more likely to extend into the intracranial
cavity through the superior orbital fissure or the
orbital roof.26 Children are at particular risk of
extension into the anterior intracranial fossa
due to lack of frontal sinus development. Medial
injuries can damage the trochlea, leading to stra-
Closed globe injuries: orbital trauma
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
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
quiescence. Glass and stone are inert materials
and are usually well tolerated within the orbit.
On the other hand, organic matter is poorly toler-
ated as it often incites a marked inflammatory
response, is more often associated with infection,
and can lead to persistent draining fistulous
tracts. Retained wooden foreign bodies can
decompose, fragment into smaller pieces, create
chronic fi stulas, migrate deeper into the orbit or
self-extrude after migrating to the surface.28
Evaluation
Metallic foreign bodies are generally well visual-
ized on CT whereas organic matter such as wood
can be mistaken for air or fat on CT. Magnetic
resonance imaging (MRI) is the imaging modal-
ity of choice for suspected intraorbital wooden
foreign bodies, but they can still be missed, par-
ticularly if small. MRI is contraindicated when
metal is suspected due to possible mobilization
of the foreign body against critical structures.
151
 Ocular trauma
Thin axial and coronal views should be obtained
to determine the exact location of the foreign
body and to assess the status of the cranial vault
and contiguous paranasal sinuses. To help guide
surgical planning, special attention should be
paid to affected structures, depth of the foreign
body, and extension into extraorbital spaces.
Extension into contiguous sinus cavities may
require a combined approach with ophthal-
mology and otorhinolaryngology. Intracranial
involvement via the superior orbital fissure, the
optic canal, or an orbital roof fracture can be
life-threatening, requires a high index of suspi-
cion to diagnose, and demands neurosurgical
intervention when discovered.26
Because the orbit converges toward its apex,
long pointed objects can be directed toward the
apex by the confi nes of the bony walls. The
deeper the foreign body penetrates, the more
likely a serious injury will result. Sometimes the
patient will have removed a deeply penetrating
foreign body prior to examination. When the
history or clinical fi ndings suggest a deep orbital
injury, a minor-appearing external wound should
not fool the examiner into overlooking a more
serious underlying injury. Vital structures such
as the optic nerve, ophthalmic artery, and sensory
and oculomotor nerves can be injured when an
object penetrates deep into the orbital apex.
Serious and permanent injury, such as meningitis
or brain abscess, can result from unrecognized
intracranial extension.26
Treatment
Indications for removal of intraorbital foreign
bodies include:
1. easily accessible anterior location
2. organic matter or copper
3. inflammatory reaction
4. sharp edges that threaten critical structures
5. impingement on extraocular muscles or nerves
causing functional deficits.
152
Indications for observation of intraorbital foreign
bodies include:
1. small, smooth, inert, posteriorly-located intra-
orbital foreign bodies
2. absence of infection or inflammation
3. lack of current or potential visual
compromise
4. high risk of iatrogenic injury during surgical
removal (hemorrhage or functional deficit)
that outweighs the benefit of removal.
When observation is elected, patients should be
monitored closely during the fi rst year for stabil-
ity. They should also be warned of the risk of
dislodgement should they ever develop an impor-
tant indication for MRI (if the foreign body is
metallic).
Intraorbital vegetable matter should be removed
expediently and thoroughly. Aggressive irriga-
tion with antibiotics and debridement of sur-
rounding tissues is vital. Intraoperative cultures
should be obtained with dirty wounds and inju-
ries involving organic material. Wounds caused
by wood (twigs, pencils, golf tees) often carry
and deposit multiple small organic particles
through the path of entry. Complete removal
can be difficult, especially since these particles
can break into smaller pieces that are poorly
imaged even with MRI and wood has a tendency
to catch on orbital tissues. Retained wooden
foreign bodies have a high incidence of granu-
loma, abscess, or fi stula formation and can be
extremely challenging to manage. It is important
to avoid pushing the decomposing and disinte-
grating pieces deeper into the orbit as they may
become more difficult to remove with subse-
quent efforts and cause iatrogenic damage.27
Prophylactic antibiotics are controversial for
small, inert intraorbital foreign bodies that are
not causing functional deficits. However, antibi-
otic prophylaxis is indicated in cases of eyewall
violation, sinocranial involvement, or exposure
to organic material.
 Closed globe injuries: orbital trauma

CASE EXAMPLES

Case report: intraorbital foreign body (Figure 10.12)

A 2-year-old boy was vacationing with his family
when he fell from a second floor balcony into a bush.
The patient was airlifted to the emergency room for
evaluation (A). Initial examination revealed a large
twig extending from the orbit just below the left
globe (B). A CT scan with contrast revealed the twig
indenting and displacing the left eye superiorly. The
patient was taken to surgery where the foreign body
was carefully removed (C) and the area thoroughly
irrigated and debrided (D). An upper eyelid marginal
laceration was repaired. Incredibly, the globe was
found to be intact. Cultures taken at the time of
surgery grew Bacillus cereus. The patient was admit-
ted for intravenous antibiotics. He steadily improved
and never developed a clinical infection. The upper
eyelid healed well and final visual acuity was 20/20.
(With permission from Johnson TE. Intraorbital
Branch. From Arch Ophthalmol 2000;118:590–591.
Copyright © 2000, American Medical Association. All
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
injuries are caused by contusive head trauma.
The most common mechanisms are motor vehicle
accidents, falls, bike accidents, and assault.29 The
incidence of optic nerve trauma as a result of
midfacial fractures is approximately 3%. 30
Most patients presenting with optic nerve
trauma are young, with a mean age of 32–34, and
approximately 81–85% are male. 31,32 Immediate
loss of vision upon impact is most common, but
some cases of delayed visual loss have been
reported. No light perception vision upon initial
examination occurs in approximately 40–48% of
cases. 31–33 A considerable number of cases are
associated with loss of consciousness with esti-
mates reported around 45%. 31 Visual loss can
include loss of central visual acuity, visual field
defects, afferent pupillary defects and color
vision defects. Profound visual loss is more
common than mild visual loss.
Pathophysiology
Damage to the optic nerve occurs by any com-
bination of the following:
1. direct deformation of the skull and optic
canal
2. shearing of the optic nerve microvasculature
3. tearing of the nerve axons
4. contusion of the nerve against the optic
canal.
The intracanalicular portion of the optic nerve
is the most vulnerable, in part owing to tethering
of the dura by the periosteum of the optic canal.
Iatrogenic optic nerve injuries can also occur
after ethmoidal endoscopic sinus surgery, 34 ret-
154
Figure 10.13 The optic atrophy seen in traumatic optic
neuropathy is delayed by several weeks. A middle-aged
male patient with a severe closed head injury had
fundus photos 3 days (left) and 3 months (right) after
the initial injury. Visual acuity was hand motions at
both visits.
robulbar anesthesia, orbital apex surgery, or
reduction of midfacial fractures.
Evaluation
By defi nition, indirect optic nerve trauma occurs
in the setting of head trauma. Therefore, patients
often have serious neurologic injury and must
be evaluated in conjunction with trauma phy-
sicians, neurosurgeons, and head and neck sur-
geons. If the patient is obtunded, the only clinical
evidence of a traumatic optic nerve injury may
be a relative afferent pupillary defect in the
absence of globe injury. Evidence of optic atrophy
is delayed ophthalmoscopically for weeks to
months following injury (Figure 10.13). However,
every attempt should be made to document
visual acuity as soon as is clinically possible
and to rule out pre-existing visual loss by history.
The diagnosis of traumatic optic neuropathy
cannot be made in the setting of normal visual
acuity or in the absence of a relative afferent
pupillary defect. While older reports in the
literature suggested that all patients with trau-
matic optic nerve injuries presented with no
light perception vision, more recent reports
indicate that while most patients have visual loss
of 20/400 or worse, some will present with mild
visual loss. Therefore, a high index of suspicion

should be maintained to identify more subtle
cases.29
Intraocular pathology may occur with or with-
out optic nerve injury and it may be difficult to
distinguish the etiology of visual loss in these
cases. However, decreased vision and abnormal
pupillary function without ocular injury is strongly
suggestive of traumatic optic neuropathy.
The diagnosis of traumatic optic neuropathy is
clinical. Radiologic examination is useful in
localizing the precise site and mechanism of
injury and in preoperative planning. Computed
tomography is superior to magnetic resonance
imaging in detailing optic canal fractures or
impingement of the optic nerve by bony frag-
ments. MRI is superior in delineating optic nerve
sheath hemorrhage. High resolution paraconal
oblique views may be necessary to distinguish
intrasheath from extradural hemorrhage.
Treatment
The optimal treatment of traumatic optic neu-
ropathy is unknown. Unfortunately, no random-
ized controlled prospective trials have been
feasible to date because of the difficulty in enroll-
ing traumatized patients, relative rarity of the
condition, and controversy over optimal treat-
ment strategies. The biochemical and patho-
physiological mechanisms of optic nerve injury
are poorly understood and our knowledge in this
area lags far behind our knowledge of brain and
spinal cord injury. It is unknown whether current
medical or surgical interventions improve the
outcome when compared to the natural history
of traumatic optic neuropathy. There is currently
no standard of care with regard to treating trau-
matic optic nerve injuries.
Management strategies currently include:
1. observation
2. high-dose corticosteroids
3. optic canal decompression.
Closed globe injuries: orbital trauma
Although older literature suggests a grave
prognosis with traumatic optic neuropathy,
more recent literature demonstrates a 20–35%
improvement rate with no treatment. 35,36
Several cases of spontaneous improvement
despite severe vision loss (no light perception)
have been reported 37 and this suggests that
severe optic nerve trauma is not always
irreversible. Observation alone may be reason-
able for some patients, particularly for those
with gastritis, diabetes, or immunosuppres-
sion as steroids can exacerbate any underly-
ing conditions and potentially lead to serious
complications (e.g. GI bleeding, diabetic
ketoacidosis).
The rationale for treatment with high-dose
steroids is based on results from the second
National Acute Spinal Cord Injury Study
(NASCIS II). NASCIS II was a multicenter,
randomized, double-blind, placebo-controlled
study. It demonstrated that patients who received
methylprednisolone (30 mg/kg initial dose
followed by 5.4 mg/kg/hr) within the fi rst 8
hours after spinal cord injury had improved
motor and sensory function when compared
to patients who received placebo, naloxone, or
high-dose steroids after 8 hours. 38 Animal
models of spinal cord injury show that pre-
treatment with high dose methylpredniso-
lone prevents free radical damage and improves
spinal cord blood flow. One animal model of
crush injury to the optic nerve showed preserva-
tion of optic nerve head blood flow when pre-
treated with dexamethasone. 39 No prospective
clinical studies similar to NASCIS II have been
feasible on patients with acute optic nerve
injuries.
High-dose methylprednisolone therapy for
traumatic optic nerve injury has recently been
called into question. Since the spinal cord is a
mixed gray and white matter tract and the optic
155
 Ocular trauma
nerve is a purely white matter tract, the clinical
benefits of high dose steroid therapy may not
translate to the optic nerve. In addition, one
recent animal study of crush injury to the optic
nerve showed a dose-dependent decline in the
number of surviving axons that were treated
with methylprednisolone,40 suggesting a poten-
tial harm of this treatment. A recent prospective
randomized controlled trial on early high-dose
methylprednisolone treatment after acute head
injury was actually ended early because cortico-
steroids were found to have an adverse effect on
survival.41 However, the mechanism by which
corticosteroids may increase mortality in the
setting of acute head trauma is unknown. In
summary, it remains unknown to date whether
high-dose methylprednisolone provides any
benefit to the acutely traumatized optic nerve.
The authors advocate using the NASCIS II
regimen only for stable patients with severe
vision loss and without systemic contraindica-
tions. If there is no visual improvement within
2–3 days, the corticosteroids should be
discontinued.
Optic canal decompression may be of benefit
to certain patients with delayed visual loss
presumably attributable to secondary mecha-
nisms of optic nerve damage. Primary damage
to optic nerve axons at the moment of injury
may be irreversible, but the subsequent cascade
of inflammation, edema, ischemia, and meta-
bolic dysregulation within the unyielding
bony optic canal may in turn further damage
surrounding axons. While no prospective studies
have proven this therapy to be clearly beneficial,
it is an accepted management strategy for
patients who have no response to high dose
methylprednisolone, cannot be tapered from
high dose methylprednisolone without loss of
vision, or have stable visual loss followed by
subacute worsening. Optic canal decompres-
sion should also be considered for optic canal
156
fractures with bony fragment impingement
of the optic nerve and for intrasheath
hemorrhages.
In the future, neuroprotective agents may rev-
olutionize the treatment of acute optic nerve
injuries. This will require a more complete
understanding of the pathophysiologic mecha-
nisms of primary optic nerve injury and second-
ary mechanisms that perpetuate the damage and
contribute to the death of surrounding yet unin-
jured axons.
It is difficult to predict an individual patient’s
prognosis following a traumatic optic nerve
injury. Although not always readily available,
flash visual evoked potentials have been shown
to have prognostic value in obtunded patients
with unilateral traumatic optic neuropathy and
in some cases may help guide management.42 It
is clear now that traumatic optic neuropathy
encompasses a spectrum of clinical outcomes
and the possibility for partial recovery is present.
A poor prognosis is associated with:
1. no light perception vision immediately after
trauma
2. advanced age
3. a large relative afferent pupillary defect42,43
4. impingement of the optic nerve by bony
fragments
5. intrasheath hemorrhage that is not promptly
evacuated.
ORBITAL HEMORRHAGE AND
COMPARTMENT SYNDROME
Introduction
Orbital hemorrhage is an uncommon entity,
but it can cause severe vision loss if managed
inappropriately. Patients typically present fol-
lowing facial trauma with pain and decreased
vision.
Trauma is the most common cause of orbital
hemorrhage. Other etiologies include:

1. Iatrogenic causes:
a. hemorrhage due to peribulbar or retrobul-
bar injection
b. post-surgical bleeding.
2. Spontaneous causes:
a. hemorrhage due to tumors
b. hemorrhage due to vascular lesions.
Traumatic orbital hemorrhages may occur by a
variety of mechanisms.2,44–50 The trauma can
either be directly to the orbit or to other
regions of the face with resulting fractures
or secondary injury to the orbit. Bleeding may
occur within several spaces contained within the
orbit including the subperiosteal, extraconal,
intraconal, or sub-Tenon’s space.45,47–50 Bleeding
can also occur within the sheath of the optic
nerve.
The orbit is susceptible to compartment syn-
drome because of its anatomy and small size. It
is essentially a closed space bound by four bony
walls and the minimally distensible orbital
septum and globe.2,50 Rapid elevation in com-
partmental pressure can be created by a rela-
tively small volume of hemorrhage since normal
orbital volume is approximately 30 cc.46 Isch-
emia of orbital tissues and increased intraocular
pressure then occur depending on the extent of
orbital hemorrhage. Orbital compartment syn-
drome is less likely in patients with extensive
orbital fractures, particularly large floor frac-
tures, as orbital contents are decompressed into
the contiguous sinuses.
Evaluation
Patients affected by orbital hemorrhage may
report a variety of symptoms including decreased
vision, pain, and diplopia.2,45,49 A multidisci-
plinary approach is often necessary when dealing
with head trauma patients. Life-threatening con-
ditions need to be ruled out and appropriate
monitoring should be in place before evaluation
of the eye begins. A thorough history regarding
Closed globe injuries: orbital trauma
the mechanism of injury should be undertaken
if possible. Ophthalmic examination may reveal
reduced visual acuity, increased intraocular pres-
sure, an afferent pupillary defect, periorbital
ecchymoses, subconjunctival hemorrhage, and
conjunctival chemosis. Proptosis and taut orbital
contents are universally present in orbital com-
partment syndrome. In severe cases, choroidal
folds or evidence of a central retinal artery occlu-
sion may be present.45 A complete eye examina-
tion is necessary to rule out concomitant ocular
injury. Imaging of the orbits with CT or MRI is
typically necessary. However, decreased vision or
an afferent pupillary defect in the presence of
apparent orbital hemorrhage implies an acute
orbital compartment syndrome. As permanent
damage to the optic nerve may result, emergent
therapy is critical, oftentimes before imaging can
be performed.45
If evidence of an optic neuropathy is present
without significant clinical evidence of a retro-
bulbar hemorrhage, a CT scan may reveal a local-
ized radiodensity surrounding portions of the
optic nerve. This may be indicative of an intra-
sheath hematoma directly compressing the optic
nerve. An MRI scan should then be performed
to confi rm the diagnosis.50 If an intrasheath
hematoma is present, the patient should emer-
gently be referred to an oculoplastic surgeon for
possible optic nerve sheath fenestration.
Treatment
The treatment of orbital hemorrhage depends on
the severity of the compartment syndrome. Mild
to moderate elevations in intraocular pressure
without evidence of optic nerve compromise
(afferent pupillary defect) can be treated with
glaucoma medications and observation. However,
if the optic nerve or retinal circulation is com-
promised, immediate defi nitive therapy is
necessary.2,45,47,50
157
 Ocular trauma
Initial emergency therapy is canthotomy and
cantholysis of the lateral canthal tendon. A thor-
ough description of this procedure is found
below. Lateral canthotomy and cantholysis works
by increasing orbital volume and allowing the
eye to move anteriorly. Success is judged by
decreased intraocular pressure, improved visual
acuity, and reversal of an afferent pupillary
defect. An inferior cantholysis is initially per-
formed. If further decompression is necessary, a
superior cantholysis can also be performed. If
the compartment syndrome is not alleviated by
these interventions, emergent consultation with
an oculoplastic surgeon is mandatory. An oculo-
plastic surgeon can further decompress the orbit
by using the following methods:
1. create a lid crease incision and open the orbital
septum
2. explore the inferotemporal orbit through an
inferior subciliary incision
3. surgically decompress the bony orbit.
Successful orbital decompression should be fol-
lowed by careful monitoring as patients may
redevelop orbital compartment syndrome if
further bleeding occurs. Lateral canthotomy and
cantholysis procedures are easily reversed by an
oculoplastic surgeon once the acute episode has
resolved.
Lateral canthotomy and cantholysis
If possible, proper informed consent is obtained.
The region of the lateral canthus should be
prepped and draped in a sterile fashion. Two
158
percent lidocaine with epinephrine is infi ltrated
into the lateral canthal region both subcutane-
ously and subconjunctivally. If possible, 15
minutes should be allowed for the epinephrine
to take effect. If cautery is available it should be
at hand. If cautery is not available, the procedure
should be performed using simple pressure for
hemostasis.
Clamping of the lateral canthus with a hemo-
stat may be performed to reduce the likelihood
of bleeding but usually is not necessary. A Stevens
scissors is placed with one blade on the conjunc-
tival side of the lateral canthus and one blade on
the skin side of the lateral canthus. Lateral pres-
sure is applied to the scissors as the canthotomy
is performed.
At this point the broad lateral canthal tendon
has been cut in half horizontally. There is little
decompression of the orbit as it has not been
separated from the lateral wall of the orbit. To
perform a complete inferior cantholysis, the infe-
rior lateral canthal tendon is strummed with the
scissors within the canthotomy wound. A fi rm,
tense, cord-like attachment will be felt. These
fi rm attachments are cut with scissors until the
lower lid becomes completely free from its lateral
attachments. This may take several snips as
the lateral canthal tendon is wide and spreads
as it approaches the lateral orbital tubercle
posterior to the lateral orbital rim. Hemostasis
is obtained. The patient is then re-examined for
improvement in signs of orbital compartment
syndrome.
 Closed globe injuries: orbital trauma

CASE EXAMPLES

Case report: orbital compartment syndrome (Figure 10.14)

A 27-year-old male with a longstanding history of
mental illness presented with decreased vision and
pain after attempting to self-enucleate his right eye.
Initial visual acuity was light perception without pro-
jection. Intraocular pressure was 60. Ophthalmic
examination revealed a total hyphema. The orbital
contents were tense and swollen (A). The lateral
canthus and surrounding areas were sterilely
prepped and draped. 2% lidocaine with epinephrine
was used for local anesthesia. Using Stevens scissors,
a lateral canthotomy was fashioned (B). After strum-
ming the inferior crus of the lateral canthus with the
scissors to correctly identify its location, an inferior
cantholysis was fashioned (C). The lateral attach-
ments of the lower lid were visibly released (D). Intra-
ocular pressure after the procedure fell to 30. Despite
the measures, the patient progressed to no light
perception vision due to massive suprachoroidal
hemorrhage.

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

160

SUMMARY
1. The thinnest bones of the orbit (lamina papy-
racea and orbital floor) are the most prone to
fracture following contusive orbital injury.
2. Blowout fractures of the orbit are a protective
mechanism to prevent undue force trans-
mitted to the globe and to decompress the
orbit.
3. Clinical examination can often diagnose
orbital fractures, but a CT scan is needed to
confi rm the diagnosis and allow appropriate
surgical planning.
4. Repair of orbital fractures is usually delayed
7–14 days after the initial injury to allow hem-
orrhage and edema to subside.
5. Indications for orbital fracture repair include
persistent diplopia, enophthalmos, or large
fractures.
6. Seemingly minor soft tissue injury can harbor
deep orbital wounds and retained foreign
bodies.
7. Traumatic optic neuropathy is a clinical diag-
nosis (relative afferent pupillary defect and
decreased vision, often with an otherwise
normal eye examination following trauma).
8. The orbit is particularly susceptible to com-
partment syndrome because of its small
volume and bony/septal enclosure.
9. Lateral canthotomy and inferior cantholysis is
the procedure of choice for vision-threatening
orbital compartment syndrome.
REFERENCES
1. Dunya IM, Rubin PA, Shore JW. Penetrating orbital trauma.
Int Ophthalmol Clin 1995;35(1):25–36.
2. Linberg JV. Orbital compartment syndromes following
trauma. Adv Ophthalmic Plast Reconstr Surg 1987;6:51–62.
3. Shakin JL, Yannuzzi LA. Posterior segment manifestations
of orbital trauma. Adv Ophthalmic Plast Reconstr Surg
1987;6:115–135.
Closed globe injuries: orbital trauma
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
Reconstr Surg 1974;54:81–82.
6. Kersten RC: Blowout fracture of the orbital floor with
entrapment caused by isolated trauma to the orbital rim.
Am J Ophthalmol 1987;103:215–220.
7. Putterman AM, Stevens T, Urist MJ. Nonsurgical management
of blow-out fractures of the orbital floor. Am J Ophthalmol
1974;77:232–239.
8. Putterman AM. Management of blow-out fractures of the
orbital floor: a conservative approach. Surv Ophthalmol
1991;35:292–298.
9. Dulley B, Fells P. Orbital blow-out fractures: to operate or not
to operate, that is the question. Brit Orthopt J 1974;31:47–54.
10. Wilkins RB, Havins WE. Current treatment of blow-out
fractures. Ophthalmology 1982;89:464–466.
11. Hawes MJ, Dortzbach RK. Surgery on orbital floor fractures:
influence of time of repair and fracture size. Ophthalmology
1983;90:1066–1070.
12. Burnstine MA. Clinical recommendations for repair of isolated
orbital floor fractures: an evidence based analysis.
Ophthalmology 2002;109:1207–1210; discussion 1210–1211;
quiz 1212–1213.
13. Jordan DR, Allen LH, White J, Harvey J, Pashby R, Esmaeli B.
Intervention within days for some orbital floor fractures:
the white-eyed blowout. Ophthal Plast Reconstr Surg
1998;14:379–390.
14. Bansagi ZC, Meyer DR. Internal orbital fractures in the
pediatric age group: characterization and management.
Ophthalmology 2000;107:829–836.
15. Egbert JE, May K, Kersten RC, Kulwin DR. Pediatric orbital
floor fracture: direct extraocular muscle involvement.
Ophthalmology 2000;107:1875–1879.
16. Sires BS. Orbital trapdoor fracture and oculocardiac reflex.
Ophthalmic Plast Reconstr Surg 1999;15(4):301–302.
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
wall fractures. Am J Ophthalmol 1984;97:349–356.
19. McLachlan DL, Flanagan JC, Shannon GM. Complications of
orbital roof fractures. Ophthalmology 1982;89:1274–1278.
20. Flanagan JC, McLachlan DL, Shannon GM. Orbital roof
fractures: neurologic and neurosurgical considerations.
Ophthalmology 1980;87:325–329.
21. Beyer CK, Fabian RL, Smith B. Naso-orbital fractures,
complications, and treatment. Ophthalmology
1982;89:456–463.
161
 Ocular trauma
22. Mauriello JA Jr, Hargrave S, Yee S, Mostafavi R, Kapila R.
Infection after insertion of alloplastic orbital floor implants.
Am J Ophthalmol 1994;117:246–252.
23. Rosen CE. Late migration of an orbital implant causing
hemorrhage with sudden proptosis and diplopia. Ophthal
Plast Reconstr Surg 1996;12: 260–262; discussion 263.
24. Simonton JT, Arthurs BP. Penetrating injuries to the orbit.
Adv Ophthalmic Plast Reconstr Surg 1987;7:217–227.
25. Fulcher TP, McNab AA, Sullivan TJ. Clinical features and
management of intraorbital foreign bodies. Ophthalmology
2002;109(3):494–500.
26. Bard LA, Jarrett WH. Intracranial complications of penetrating
orbital injuries. Arch Ophthalmol 1964;71:332–343.
27. Liu D, Al Shail E. Retained orbital wooden foreign body:
a surgical technique and rationale. Ophthalmology
2002;109(2):393–399.
28. Wesley RE, Wahl JW, Loden JP, Henderson RR. Management
of wooden foreign bodies in the orbit. South Med J
1982;75(8):924–926, 932.
29. Steinsapir KD, Goldberg RA. Traumatic optic neuropathy.
Surv Ophthalmol 1994;38(6):487–518.
30. Ashar A, Kovacs A, Khan S, Hakim J. Blindness associated with
midfacial fractures. J Oral Maxillofac Surg 1998;56(10):1146–
1150; discussion 1151.
31. Levin LA, Beck RW, Joseph MP, et al. The treatment of
traumatic optic neuropathy: the International Optic Nerve
Trauma Study. Ophthalmology 1999;106(7):1268–1277.
32. Levin LA, Joseph MP, Rizzo JF, 3rd, Lessell S. Optic canal
decompression in indirect optic nerve trauma.
Ophthalmology 1994;101(3):566–569.
33. Mauriello JA, DeLuca J, Krieger A, Schulder M, Frohman L.
Management of traumatic optic neuropathy: a study of 23
patients. Br J Ophthalmol 1992;76(6):349–352.
34. Neuhaus RW. Orbital complications secondary to endoscopic
sinus surgery. Ophthalmology 1990;97(11):1512–1518.
35. Seiff SR. High dose corticosteroids for treatment of vision loss
due to indirect injury to the optic nerve. Ophthalmic Surg
1990;21(6):389–395.
36. Lessell S. Indirect optic nerve trauma. Arch Ophthalmol
1989;107(3):382–386.
37. Wolin MJ, Lavin PJ. Spontaneous visual recovery from
traumatic optic neuropathy after blunt head injury.
Am J Ophthalmol 1990;109(4):430–435.
162
38. Bracken MB, Shepard MJ, Collins WF, et al. A randomized,
controlled trial of methylprednisolone or naloxone in the
treatment of acute spinal-cord injury. Results of the Second
National Acute Spinal Cord Injury Study. N Engl J Med
1990;322(20):1405–1411.
39. Lew H, Lee SY, Jang JW, et al. The effects of high-dose
corticosteroid therapy on optic nerve head blood flow in
experimental traumatic optic neuropathy. Ophthalmic Res
1999;31(6):463–470.
40. Steinsapir KD, Goldberg RA, Sinha S, Hovda DA.
Methylprednisolone exacerbates axonal loss following
optic nerve trauma in rats. Restor Neurol Neurosci
2000;17(4):157–163.
41. Roberts I, Yates D, Sandercock P, et al. Effect of intravenous
corticosteroids on death within 14 days in 10008 adults with
clinically significant head injury (MRC CRASH trial):
randomised placebo-controlled trial. Lancet
2004;364(9442):1321–1328.
42. Holmes MD, Sires BS. Flash visual evoked potentials predict
visual outcome in traumatic optic neuropathy. Ophthalmic
Plast Reconstr Surg 2004;20(5):342–346.
43. Alford MA, Nerad JA, Carter KD. Predictive value of the initial
quantified relative afferent pupillary defect in 19 consecutive
patients with traumatic optic neuropathy. Ophthal Plast
Reconstr Surg 2001;17(5):323–327.
44. Stern JH, Meyer DR. Orbital barotrauma. Ophthal Plast
Reconstr Surg 1995;11(1):49–53.
45. Bains RA, Rubin PA. Blunt orbital trauma. Int Ophthalmol Clin
1995;35(1):37–46.
46. Krohel GB, Wright JE. Orbital hemorrhage. Am J Ophthalmol
1979;88(2):254–258.
47. Liu D. A simplified technique of orbital decompression for
severe retrobulbar hemorrhage. Am J Ophthalmol
1993;116(1):34–37.
48. McIlwaine GG, Fielder AR, Brittain GP. Spontaneous recovery
of vision following an orbital haemorrhage. Br J Ophthalmol
1989;73(11):926–927.
49. Petrelli RL, Petrelli EA, Allen WE, 3rd. Orbital hemorrhage with
loss of vision. Am J Ophthalmol 1980;89(4):593–597.
50. Rubin PA, Bilyk JR, Shore JW. Management of orbital trauma:
fractures, hemorrhage, and traumatic optic neuropathy.
Focal Points 1994;XII(7):1–17.

Open globe injuries:
ruptures and lacerations
Daniel M. Miller, Charles W.G. Eifrig, James T. Banta
INTRODUCTION
In this chapter we will review the classification,
epidemiology, evaluation, and management of
globe ruptures and lacerations. Case examples
will reinforce key evaluation and management
points.
Guidelines for classifying mechanical eye inju-
ries were fi rst made uniform in the mid-1990s.1
A globe rupture refers to a full-thickness eyewall
wound caused by a blunt object, while a lacera-
tion refers to a full-thickness eyewall wound
caused by a sharp object. Specifics on the
classification of ocular trauma can be found in
Chapter 4. In this chapter we will discuss only
globe ruptures and lacerations. Intraocular
foreign bodies are covered in Chapter 12.
EPIDEMIOLOGY
It is difficult to estimate the number of open
globe injuries in the United States because of
significant variability in case reporting. However,
the involvement of an increasing number of
hospitals and physicians in the World Eye Injury
Registry (WEIR) will continue to improve our
understanding of the incidence and prevalence
of open globe injuries.
A review of the National Hospital Discharge
Surveys (NHDS) from 1984 to 1987 revealed an
incidence of approximately 4.6/100 000/year for
open globe injuries.2 In a smaller series in Alle-
gheny County, Pennsylvania, the incidence of
open globe injury was 3.5/100 000/year between
11
1980 and 1986. 3 The economic impact, particu-
larly when considering loss of work days due to
injury, is immense.
The age distribution of severe ocular injury is
bimodal. Young males comprise the majority of
open globe injuries with patients aged between
15 and 34 years old representing nearly one half
of all open globe injuries.2,4,5 The second peak is
seen in those over the age of 75.2,3,6 Falls are
more common in this age group. Prior ocular
surgery is also more common in the older popu-
lation and may lower the threshold of force
needed for a globe rupture to occur. For example,
a contusive injury to an eye that has previously
undergone extracapsular cataract extraction,
trabeculectomy, or penetrating keratoplasty may
be more likely to cause rupture (Figure 11.1).
PATHOPHYSIOLOGY
Distinct mechanistic differences exist between
ruptures and lacerations, and these differences
have significant bearing on evaluation, operative
planning, and repair. Ruptures are normally
caused by blunt objects, have stellate, ragged
edges and frequently create significant intrao-
cular disruption. Conversely, lacerations are
caused by sharp objects, have cleaner edges, and
cause less intraocular disruption than com-
parably sized ruptures. Rupture sites are usually
located at the weakest point of the sclera. Figure
11.2 shows the most common sites of globe
rupture. Surgeries with long incisions (extra-
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 11.2 Globe ruptures most commonly occur just
posterior to the insertion of the rectus muscles (red).
Other common sites include previous surgical sites,
particularly extracapsular cataract surgery (blue) or
penetrating keratoplasty (yellow).
wounds in particular) are prone to rupture,
but even small incision surgical sites can
rupture depending on the mechanism of injury
(Figure 11.3).
164
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
to the ophthalmic injury.
The fi rst step in evaluating a patient with a
presumed open globe injury is a thorough history.
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
with a lacerating injury, it is important to ascer-
tain whether the inciting object was removed,
displaced, or is in multiple pieces (e.g. shattered
glass). In particular, it is critical to determine if

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
surgical history should be investigated and
documented. Pre-existing ophthalmic disease
and prior ocular surgery may be relevant to
the current injury or affect the surgical plan.
Drug allergies should be documented carefully.
Finally, the time of the patient’s last oral intake
is relevant to the timing of any surgical
intervention.
A complete evaluation of the injured eye should
then be performed. Fear and caution typically
accompany an examination of a known open
globe injury as well as the potentially open globe.
Early in an ophthalmic career, the concern
centers on possibly missing an open globe injury.
Systematic and complete eye examinations will
prevent this error. The second component of
concern involves inadvertently expressing globe
contents through a rupture or laceration site.
Although this is a valid concern and all precau-
tions should be made to prevent excessive manip-
ulation of the eye and orbit, it is truly rare that
an eye will be ‘over-examined’ to the point
where globe contents are put at risk. If anything,
passivity with a potentially open globe could
lead to a missed diagnosis. It is equally important
to remember that a comprehensive examination of
the uninjured eye is critical and must never be rel-
egated to another time. Unrecognized injuries can
and do occur in a seemingly ‘uninvolved’ eye.
Open globe injuries: ruptures and lacerations
Figure 11.4 Video capture of massive extrusion of
uveal contents (primarily retina) through a large
corneal laceration. In this instance, minimal
examination was necessary preoperatively. The eye was
covered with a metal shield until the time of surgery.
Common sense must play a significant role
when examining a severely injured eye. In the
case of an extensive globe rupture or laceration
with obvious and extensive extrusion of intra-
ocular contents (Figure 11.4), a visual acuity,
pupillary examination, and slit lamp examina-
tion can be performed on the injured eye. A
metal shield is then placed over the eye until
further imaging studies (if necessary) and surgi-
cal intervention are undertaken. Again, the
uninjured eye must always be thoroughly exam-
ined for a possible unrecognized injury.
Depending on the mechanism of injury, signifi-
cant periorbital swelling can make ocular exami-
nation very difficult. The use of eyelid retractors
(e.g. Desmarres retractors) can allow safe visu-
alization of the eye without causing unnecessary
pressure on the globe (see Chapter 3). Often, a
trained staff member will hold the retractors
while the examination is being performed by the
ophthalmologist.
Visual acuity and pupillary examinations
are vital and should be assessed at initial
165
 Ocular trauma
presentation. Vision less than 20/400 and/or the
presence of a relative afferent pupillary defect
(RAPD) often coexist with an occult globe
rupture.7,8 A patient’s inability to provide an
accurate visual acuity due to I.V. sedation, intu-
bation, or intoxication should be documented in
the medical record. Visual acuity can be checked
with standard Snellen acuity in an eye examina-
tion room, but a near acuity card may be used if
the examination is in another setting. It is critical
to obtain the most accurate visual acuity possi-
ble, as initial visual acuity is an important prog-
nostic indicator. Visual acuity should be measured
with spectacles when possible. Pinhole acuity
should be recorded if spectacles are unavailable.
In eyes with severely limited visual acuity, the
perception of hand motions should be tested in
all four quadrants of peripheral vision. If hand
motions vision is not found, perception of light
should be assessed with a bright light source (e.g.
indirect ophthalmoscope). The differentiation
between light perception and no light perception
is very important, so the uninvolved eye should
be completely occluded to prevent any test
errors.
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
the case of obvious globe rupture or laceration.
166
When there is no obvious laceration or rupture
after slit lamp examination, the IOP should be
measured, as relative hypotony is a key fi nding
in the diagnosis of an occult open globe. We
recommend that an ophthalmologist perform
IOP measurement in the setting of a potential
open globe. Anterior-to-posterior pressure on
the globe or orbit should be minimized.
A thorough slit lamp examination is then per-
formed. The slit lamp exam is particularly helpful
in diagnosing an open globe in the absence of an
obvious rupture or laceration site. Several spe-
cific examination fi ndings are often seen in this
setting:
1. 360 degrees of subconjunctival hemorrhage.
2. 360 degrees of profound conjunctival chemo-
sis, also known as ‘jelly-roll’ chemosis (Figure
11.5).
3. Relative asymmetry in anterior chamber (AC)
depth. If the globe violation is anterior to the
ciliary body, the injured AC is frequently
shallow, often with peaking of the iris towards
the wound (Figure 11.6). If the full-thickness
injury occurs in the posterior segment, the
AC is frequently deeper than the fellow eye.
Figure 11.5 ‘Jelly-roll’ chemosis is frequently associated
with open globe injuries.

Figure 11.6 A 23-month-old girl was accidentally
poked in the eye by her sister while on an airplane.
Examination revealed a peaked iris with iris
incarceration through a corneal laceration. A small
hyphema was also noted.
4. Transillumination defects of the iris can reveal
the path of small projectile injuries, often
associated with perforations or intraocular
foreign bodies.
5. Violation of the lens capsule or focal cataract
formation can herald an open globe injury.
It is sometimes difficult to determine if an
anterior laceration of the cornea or sclera is full
or partial thickness. In this case a Seidel test is
performed. The eye is anesthetized. A fluores-
cein strip is dampened with sterile saline or
topical anesthetic. At the slit lamp under cobalt
blue light, the fluorescein strip is used to paint a
dense coating of fluorescein over the wound. If
the wound is full thickness, a rivulet of aqueous
will break through the fluorescein and cascade
down the surface of the eye with a very charac-
teristic appearance (Figure 11.7).
A dilated examination of the injured eye is
critical to rule out vitreous hemorrhage, intra-
ocular foreign body, retinal detachment, and
other concomitant posterior segment injuries. If
the possibility of a retained intraocular foreign
body exists, further imaging tests are manda-
tory. The following chapter discusses the diag-
nostic workup of a potential intraocular foreign
body in detail. Opaque media (e.g. total cataract
Open globe injuries: ruptures and lacerations
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-
times aid in the diagnosis. Ocular ultrasound can
be utilized in carefully selected cases provided
the manipulation of the globe is minimal and the
facilities and trained technicians are available.
Ultrasound has the advantage of providing spe-
cific anatomic information about the posterior
segment including the presence or absence of
retinal detachment, choroidal hemorrhage, and
intraocular foreign bodies. Computed tomogra-
phy (CT) is better for ruling out metallic intra-
ocular foreign bodies, but offers less specific
anatomic information. Perforating injuries are
unique in that the fi nal resting place of the
injuring object must be localized. Most objects
remain within the orbital confi nes, but exten-
sion into the sinuses or even into the brain is
possible.
Neither ultrasound nor CT is adequate to
completely rule out an occult eyewall violation.
If suspicion is high, surgical exploration is neces-
sary. Our experience suggests that when explor-
atory surgery is undertaken in questionable cases,
an eyewall violation is found in the vast majority
of cases.
Finally, it is crucial to exclude any concomitant
injuries to the lids, periorbital area, face, or head.
Concurrent orbital and adnexal injuries have
been reported to occur in 25.7% of patients with
open globe injuries. 9
Pediatric evaluation deserves a special mention.
The normal difficulties encountered when exam-
ining young patients are often magnified in the
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
child with a potentially open globe. In the
authors’ experience, children often ‘grasp’ the
gravity of the situation and with the supportive
encouragement and participation of family
members, a brief yet adequate examination can
often be performed at the slit lamp. However,
maneuvers normally employed to examine an
uncooperative child must be avoided in case an
open globe is present. In this situation, an exam-
ination under anesthesia (EUA) is often required
to diagnose and potentially repair a full-
thickness eyewall injury. The potentially injured
eye should always be shielded while preparations
for surgical exploration and/or repair are being
made.
PREOPERATIVE MANAGEMENT
AND COUNSELING
After the examination is complete and the
surgical plan is being formulated, avoid further
manipulation of the eye.10 A protective shield
(e.g. Fox shield) is placed over the injured eye
(Figure 11.8) and the patient is instructed not to
eat or drink. Most anesthesia fasting guidelines
require no food or drink for a minimum of 6
hours before general anesthesia. According to

168

Figure 11.8 After confirmation of an open globe injury
(pictured in Figure 11.6), a metal eye shield is taped
into position to prevent further manipulation.
the American Academy of Anesthesiologists’
practice guidelines, a 6-hour fasting period for
a light meal and an 8-hour fasting period for a
meal consisting of meat, milk or fried foods
is recommended.11–14 However, many reports
support more liberal fasting guidelines in both
the adult and pediatric populations.11–14
Tetanus prophylaxis is generally recommended
if not current.15 If the globe is severely ruptured
and disorganized with extensive loss of tissue
and the vision is no light perception, a primary
enucleation can be considered. Not uncommonly,
the patient may be in a poor psychological and/
or physical state or even mentally impaired from
illicit drugs or alcohol. The authors rarely recom-
mend primary enucleation except in extreme
cases with severe loss of tissue that cannot be
closed primarily (e.g. gunshot wounds). At a
minimum, attempted repair will allow the
patient time to understand the extent of injury
and be better prepared for the psychosocial
aspects of enucleation.
Primary repair of open globe injuries should be
performed urgently, but timing may be deter-
mined by the extent of ocular involvement, con-
comitant bodily injuries, general health status,
and operating room availability. Most studies
have shown no significant difference in fi nal
Open globe injuries: ruptures and lacerations
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
be a reduced visual prognosis.5 Intraocular
foreign bodies should be removed promptly
because of the increased risk of endophthalmitis
(see Chapter 12).
Local or general anesthesia may be utilized
depending on the mechanism of injury, the
extent of ocular injury, and the presence of coex-
isting medical injuries. The use of periocular
anesthesia in ocular trauma is safe if performed
with careful case selection.17,18 Generally, the
authors prefer peribulbar anesthesia for adult
patients with smaller anterior wounds without
extensive uveal incarceration. All pediatric
patients and more extensive open globe injuries
require general anesthesia.
Systemic antibiotics are recommended for
open globe injuries unless the wound is small,
well approximated, clean, and negative by Seidel
testing. Typically, prophylactic intravenous anti-
biotics consisting of vancomycin and a third
generation cephalosporin are used to cover
the most common gram positive and negative
bacteria associated with post-traumatic endo-
phthalmitis.19 Vitreous penetration of these anti-
biotics following trauma is adequate for most
gram positive organisms.20,21 Oral antibiotics
that have good vitreous and intraocular penetra-
tion may be considered in outpatient settings,
particularly fluoroquinolones.22,23 Generally, our
patients receive intravenous vancomycin and cef-
tazidime preoperatively followed by an oral
fluoroquinolone and fortified topical antibiotics
postoperatively.
169
 Ocular trauma
The patient presenting with a severe ocular
injury has just incurred a potentially life-chang-
ing event. The potential for a permanent loss of
vision and its attendant psychosocial issues must
be fully grasped by the surgeon and an appropri-
ately frank discussion with the patient and family
must be undertaken.24 Realistic goals and a
guarded prognosis are topics to be broached
before surgery.
The Ocular Trauma Score was developed to
provide an objective guideline that predicts the
likelihood of visual recovery after severe eye
injury.10 Ocular Trauma Score tables can be
posted in the examination rooms for easy refer-
ence and are helpful in providing patients and
families with concrete, objective data. The tables
can be seen in Chapter 4.
SURGICAL MANAGEMENT
Repair of corneal lacerations, corneal–scleral
lacerations, scleral lacerations and globe ruptures
involves similar perioperative considerations.
After sterile preparation of the eye, carefully
avoiding undue pressure to the globe, the
authors examine the eye under the operating
room microscope and devise a surgical strategy.
The goal of primary repair for an open globe
injury, whether rupture, penetration or perfora-
tion, is to:
1. close the globe with minimal manipulation
2. reposit or excise exposed intraocular
contents
3. explore the globe for unrecognized injuries
4. decrease the risk of endophthalmitis and
maximize the chance of functional recovery
by restoring ocular integrity.
Obvious lacerations or rupture sites should be
repaired fi rst, usually proceeding from anterior
to posterior. The specifics of instrumentation
170
and surgical repair are described below within
each category of laceration or rupture.
Corneal lacerations
Small, self-sealing, clean corneal lacerations
without iris incarceration or other ocular injuries
may be closed with cyanoacrylate glue.25 In our
experience, this represents a small subset of
corneal lacerations. However, it may be an effec-
tive way to stabilize a wound without a trip to
the operating room. The key to this technique is
to apply a uniform amount of glue to the wound.
We utilize a combination of a cotton swab, baci-
tracin ointment, and fi lter paper or plastic surgi-
cal drape to serve as the glue applicator. By gently
pressing on the cornea with this applicator the
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
and topical antibiotics are prescribed. Close
observation is mandatory to make certain the
glue stays in place and the eye remains formed
and free of infection.
For larger or more complicated corneal lacera-
tions, surgical management is required. The fi rst
step involves creating a limbal paracentesis site
with a paracentesis blade. A cohesive viscoelastic
(preferred because of its easy removal without Included
on DVD
extensive turbulence or vacuum) is injected
through the paracentesis to stabilize the anterior
chamber, viscodissect iris incarcerated from
the wound, and protect the corneal endothelium
and crystalline lens. Hyperinflation should be
avoided, particularly if the possibility of a pos-
terior rupture exists. A cyclodialysis spatula or
the viscoelastic cannula is then inserted through
the paracentesis to free incarcerated iris or break
adhesions. Balanced salt solution may also be
used to irrigate through the wound and free
incarcerated iris. If uvea appears necrotic or does
not reposit easily, excision may be required.

A 10-0 Nylon suture
B the long pass and equal length on each side of the
Figure 11.9 A small amount of bacitracin ophthalmic
ointment placed on the end of a sterile cotton swab
acts as an adhesive to which a thin disk of surgical
drape, or, as in this case, pre-cut filter paper is attached.
A thin, even layer of cyanoacrylate glue is then placed
on the surface of the filter paper. The glue is then
applied gently to the corneal wound (A). Once
removed, the thin, uniform layer of glue is seen closing
the wound (B). A large scleral contact lens is then
placed to prevent inadvertent dislodging of the glue.
Once the wound is free of uvea, closure of the
wound commences. 10-0 nylon suture is recom-
mended for corneal lacerations and should begin
with a central suture. The wound is then divided
Open globe injuries: ruptures and lacerations
Cornea Corneal laceration
Figure 11.10 Appropriate architecture and depth of
corneal sutures during corneal laceration repair. Note
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
less postoperative astigmatism than short, tight
sutures. The nylon sutures should be rotated and
buried once the wound is stabilized and the eye
can maintain an adequate intraocular pressure.
Viscoelastic is gently irrigated out of the anterior
chamber at the completion of surgical repair.
Once the corneal laceration is repaired, proceed
to further globe exploration if warranted (see
Ruptured globe repair, below). Subconjunctival
antibiotic and steroid is given upon completion
of the case. Topical antibiotic or combination
antibiotic/steroid drops or ointment may be
applied before the eye patch and shield are
placed.
171
Ocular trauma
CASE EXAMPLES
Case report: corneal laceration (Figure 11.11)
A 38-year-old Hispanic male was working on his car
when he felt something strike his left eye. He was not
wearing protective eyewear. He reported immediate
discomfort and decreased vision. Initially, he was
evaluated at an outside emergency room. Informa-
tion obtained during this emergency room assess-
ment included an orbital CT scan that did not
demonstrate an intraocular foreign body. He was
subsequently transferred for further evaluation and
treatment.
On presentation, the patient’s visual acuity was
20/20 and hand motions in the right and left eye
respectively. No relative afferent pupillary defect
was detected. A complete examination of the right
eye including a dilated fundus examination was
within normal limits. Slit lamp examination of the
left eye revealed an extensive L-shaped corneal
laceration with uveal prolapse and 80% hyphema.
Intraocular pressure measurement was deferred. The
iris, crystalline lens, and posterior segment were
poorly visualized through the hyphema and uveal
prolapse. A B-scan ultrasound was obtained and
demonstrated diffuse fundus thickening with scleral
folds, inferior vitreous opacities consistent with
posterior dislocation of the crystalline lens and
A B
172
hemorrhage (A). No retinal tear or detachment was
identified.
The patient was admitted to the hospital, intrave-
nous antibiotics were initiated, tetanus immuniza-
tion was given, and surgical consent was obtained.
The patient then underwent corneal laceration
repair and uveal repositioning. No intravitreal anti-
biotics were administered. He was treated with
topical fortified vancomycin and tobramycin in the
first week postoperatively. He did not develop signs
or symptoms of endophthalmitis. The corneal lacera-
tion was well approximated following surgical repair
(B).
He had a diffuse vitreous hemorrhage after primary
repair and a follow-up B-scan demonstrated a supe-
rior retinal detachment (C). A vitreoretinal surgeon
was consulted and the patient underwent a second-
ary procedure to remove the crystalline lens and
repair the retinal detachment. A month later (just
before suture removal), anterior segment examina-
tion revealed a well-healed corneal scar, extensive
loss of the temporal iris, and aphakia (D). However,
his retina remained attached and final best-
corrected visual acuity was 20/30 (with a rigid
gas-permeable contact lens).

Case report: corneal laceration (cont’d)
C D
Corneal–scleral laceration
Included
on DVD This is typically a larger wound with a higher
incidence of uveal prolapse or incarceration. The
primary objective is to fi rst stabilize the limbus
by placing a 9-0 nylon suture, thereby restoring
the anatomy of the limbal ring. Once this is
accomplished, repositing prolapsed uvea or
relieving incarceration is possible utilizing the
techniques described above. We generally repair
in an anterior to posterior direction after the
limbus is stabilized. Closing the scleral portion
of the laceration will be discussed in the follow-
ing paragraph.
Scleral laceration
Scleral wounds must be addressed with a high
index of suspicion for a more extensive disrup-
tion of ocular anatomy and prolapse of intraocu-
lar contents. The posterior extent of the laceration
must be identified. Overlying conjunctival and
Tenon’s attachments are often edematous and
adherent to the wound edges, obscuring the
extent of the laceration. It is critical to dissect
conjunctiva and Tenon’s with forceps and
blunt Westcott scissors so the posterior extent of
Open globe injuries: ruptures and lacerations
the scleral wound is completely visualized.
Scleral wounds require a larger caliber suture,
typically 8-0 or 9-0 nylon. Large scleral lacera-
tions often have significant prolapsed uveal tissue
that prohibits easy closure of the wound. Place-
ment of one or two central sutures can stabilize
the wound and allow more controlled reposition
of prolapsed uveal contents. Toothed forceps
(0.12) are used to grasp the edge of the wound
while the suture is passed. Suture passes should
be at least 50% depth, and full-thickness passes
should be avoided. Interrupted sutures are
preferred, and the ends are cut and rotated if
possible.
A scleral laceration may extend underneath or
through a rectus muscle. In this case, the rectus
muscle may be secured with a double-armed 5-0
Vicryl suture and disinserted from the globe (as
in standard strabismus surgery). The detached
muscle is carefully secured away from the opera-
tive field by marking the attached sutures with
a bulldog-style clamp. Once the wound is closed,
a disinserted rectus muscle can be secured back
to its original insertion site with the pre-placed
double-armed suture.
173
 Ocular trauma
Posterior scleral lacerations are technically
more challenging. It may be necessary to perform
a 360 degree conjunctival peritomy, isolate the
four rectus muscles on muscle hooks, and secure
each with a loop of 2-0 braided polyester suture.
This will permit maximal surgical exposure of
the wound. To prevent further prolapse of uveal
tissue, it is critical to limit torque or pressure on
the globe while the laceration is open. If the
wound continues posteriorly past the equator,
complete closure of the wound may be difficult,
especially since extensive manipulation may
lead to expulsion of ocular contents. In this
setting, the most posterior portion of the wound
may be left to heal by secondary intention.
If there is tissue loss, a scleral or corneal patch
graft is an option and should always be con-
sidered in the preoperative assessment (so appro-
priate arrangements can be made with the eye
bank).
If the mechanism of injury suggests a possible
perforating wound, exploration for both the
entry and exit wounds is mandatory. Frequently,
the more anterior wound is discovered and closed
fi rst. Exploration is then performed in the same
fashion as described above with isolation of each
rectus muscle and gentle exploration of each
quadrant until the second wound (usually the
exit wound) is found and closed.
The conjunctiva is closed with an absorbable
suture. The authors prefer 6-0 plain gut or 7-0
Vicryl. Subconjunctival antibiotics are given and
peribulbar anesthesia may be administered for
postoperative pain control (particularly helpful
in children).
174
Ruptured globe repair
The repair of a globe rupture is similar to what
has previously been described for lacerations of Included
on DVD
the cornea and sclera. Typically, ruptures are
technically more challenging to repair since
stellate wounds, extensive loss of intraocular
contents, and loss of tissue are much more
common. Oftentimes, exploratory surgery is
necessary before the rupture site is located
since ruptures are often masked by extensive
hemorrhage and chemosis. A conjunctival perit-
omy is performed in the area of suspicion using
forceps and blunt Wescott scissors, carefully
dissecting until reaching the rupture site. If the
site of the wound is unknown, the peritomy is
performed 360 degrees for maximum exposure.
Bipolar cautery may be needed for hemostasis.
It is critical to completely dissect away conjunc-
tiva and Tenon’s attachments so that all aspects
of the wound are visible. A muscle hook may be
needed to help maneuver the eye for proper
exposure but extreme caution is warranted to
prevent further extrusion of intraocular con-
tents. Suture selection can vary and depends on
the wound size, tissue loss, and location of
rupture. The authors prefer using 8-0 or 9-0
interrupted nylon suture. Once the wound is
found, it is closed in the same fashion as scleral
lacerations described above.
Rarely, in cases of severe contusive trauma, a
circumferential rupture may exist that encircles
a significant portion of the globe and passes
beneath multiple rectus muscles. These injuries
require extensive dissection and disinsertion of
multiple rectus muscles before the wound can be
adequately accessed and closed.

CASE EXAMPLES
Case report: globe rupture (Figure 11.12)
A 34-year-old white male was assaulted with a beer
bottle 2 days prior to presentation. The patient
reported immediate decreased vision and pain in
the left eye. He was initially assessed at an outside
emergency room where an orbital CT scan ruled out
an intraocular foreign body. He had no significant
medical or ophthalmic history.
On presentation his visual acuity was 20/20 OD and
light perception OS. Thorough examination of the
right eye was normal. External examination revealed
periorbital erythema, swelling, and multifocal skin
lacerations (A) around the left eye. Intraocular pres-
sures were 18 and 5 in the right and left eyes respec-
tively. Anterior segment examination of the left eye
revealed no obvious corneal or scleral lacerations.
A B
C D
Open globe injuries: ruptures and lacerations
However, globe rupture was suspected because of
the asymmetric intraocular pressure, 360 degrees of
subconjunctival hemorrhage (B), and an asymmetri-
cally deep anterior chamber (C) compared to the
right eye. Examination of the posterior segment
revealed only dense vitreous hemorrhage. The
patient was consented for globe exploration and
possible ruptured globe repair. At the time of surgery,
a 360 degree conjunctival peritomy was fashioned
and muscle hooks were used to isolate the rectus
muscles. A large rupture was identified starting
beneath the insertion of the superior rectus and
traveling circumferentially around the globe to
beneath the lateral rectus insertion. The total length
of the wound was 17 mm. There was uvea,
175
 Ocular trauma
Case report: globe rupture (cont’d)
vitreous, and retina prolapsed through the wound.
Intraocular tissues were carefully reposited and the
wound was closed primarily with interrupted 8-0
nylon sutures.
His visual acuity remained light perception post-
operatively. Follow-up echography demonstrated a
POSTOPERATIVE MANAGEMENT
On the fi rst day after surgery, full clinical exami-
nation is performed including intraocular pres-
sure check and dilated fundus examination. A
Seidel test is performed on the wound if pos-
sible. Topical antibiotic, steroid and cycloplegic
drops are recommended. Aqueous suppressants
are used if intraocular pressure is elevated.
The eye is shielded and recommendations to
avoid strenuous activity are given. Oral antibiot-
ics, typically a fluoroquinolone, are continued.
Follow-up is scheduled depending on the mecha-
nism, extent, and cleanliness of the inciting
injury as well as the postoperative appearance
and intraocular pressure. Frequent follow-up is
needed in the case of uncontrolled intraocular
pressure or a case deemed high risk for post-
traumatic endophthalmitis. Small clean wounds
with a good postoperative appearance can be
followed in a week. Vitreoretinal consultation
after primary repair is recommended in cases
with an intraocular foreign body, endophthalmi-
tis, retinal detachment, posterior scleral rupture
or laceration, vitreous hemorrhage, hemorrhagic
choroidal detachments, or a dislocated lens.
Further descriptions of secondary surgery and
further restoration of normal anatomy is beyond
the scope of this text.
176
total, complex retinal detachment (D). Vitreoretinal
consultation was obtained and the patient subse-
quently underwent extensive posterior segment
surgery to repair the retina and remove the cry-
stalline lens. Postoperatively, the retina remained
attached, but vision remained hand motions.
Corneal sutures are normally removed at the
slit lamp 1 month after primary repair. If second-
ary procedures are necessary, suture removal can
often be performed simultaneously.
Special consideration is necessary for the post-
operative care of pediatric patients. Depending
on the age of the patient, removal of sutures
often requires general anesthesia. Amblyopia is
a feared outcome in children under the age of
10, even with an excellent anatomic result. Once
the acute phase following injury and repair has
passed, consultation with a pediatric ophthal-
mologist is encouraged so that appropriate
amblyopia management can be undertaken.
COMPLICATIONS AND OUTCOMES
As discussed previously, the Ocular Trauma
Score can be helpful in preoperative counseling
and prognostication. Multiple studies have
defi ned variables related to visual outcomes fol-
lowing open globe injury. Initial visual acuity has
been shown to be a good predictor of visual
outcome in open globe injuries.27 The length
and/or width of the laceration or rupture has
been shown to correlate with outcomes as
well.28–33 In addition, lacerations posterior to the
rectus muscles, vitreous hemorrhage, involve-
ment of the crystalline lens, and the develop-
 Open globe injuries: ruptures and lacerations

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
signs.28–33
Endophthalmitis following open globe injury is
a feared complication. The incidence of trau-
matic endophthalmitis after penetrating ocular
trauma is low, occurring in approximately 5–14%
of eyes. 34–40 The risk factors portending a greater
risk of endophthalmitis include intraocular
foreign bodies, delay in wound closure greater
than 24 hours, injury in a rural setting, and dis-
ruption of the crystalline lens.34–40 The most
common organisms causing post-traumatic endo-
phthalmitis are Bacillus species, Staphylococcus
species, and other gram positive cocci. 34–40 Pro-
phylactic intravitreal or intracameral injection of
antibiotics (ceftazidime and vancomycin) is con-
sidered in patients with an intraocular foreign
body or a potentially contaminated wound.
Traumatic endophthalmitis is discussed in detail
in Chapter 13.
Sympathetic ophthalmia is a rare granuloma-
tous inflammatory disorder that usually occurs
following ocular trauma. In these rare instances,
the injured eye incites an inflammatory response
in the unaffected eye and can cause permanent
loss of vision. In a severely injured eye with little
or no visual potential, the risk of sympathetic
ophthalmia must be discussed with the patient
and be part of the decision-making process. The
specifics of sympathetic ophthalmia are dis-
cussed in detail in Chapter 13.
Isolated corneal lacerations often have a better
prognosis than more extensive corneoscleral lac-
erations and ruptures. However, corneal scars
following laceration repair often lead to irregular
astigmatism and frequently involve the visual
axis (Figure 11.13). Rigid gas-permeable (RGP)
contact lenses can often dramatically improve
vision, even when the visual axis is involved. If
an RGP contact lens is unsuccessful, penetrating
keratoplasty is often required for visual
rehabilitation.
CONCLUSIONS
Open globe injury is one of the more harrowing
diagnoses an ophthalmologist will face. A sys-
tematic approach to an injured eye is mandatory.

177
 Ocular trauma
Proper classification, examination, counseling,
repair, and postoperative management are im-
portant to restore the eye’s anatomic integrity
and potential function. Despite appropriate
intervention, the overall visual prognosis for
open globe injuries is very guarded. Prevention
remains the best treatment for all severe ocular
injuries.
SUMMARY
1. Proper classification of open globe injuries has
a direct impact on surgical planning and
procedures.
2. A complete and systematic examination of an
injured eye will prevent missing the diagnosis
of an open globe.
3. Never ignore the fellow, seemingly uninjured
eye.
4. Specific examination fi ndings can aid in the
diagnosis of the open globe without a visible
laceration or rupture (see Evaluation).
5. Perioperative planning (e.g. intravenous anti-
biotics, type of anesthesia, timing of surgery)
for the repair of an open globe injury varies
depending on the type and cleanliness of
injury as well as the patient’s medical
history.
6. Surgical repair of the open globe strives to
restore normal anatomy with minimal intra-
operative manipulation.
REFERENCES
1. Pieramici DJ, Sternberg P, Aaberg TM, et al. A system for
classifying mechanical injuries of the eye (globe). Am J
Ophthalmol 1997;123:820–831.
2. Klopfer J, Tielsch JM, Vitale S, See L-C, Canner JK. Ocular
trauma in the United States: eye injuries resulting in
hospitalization, 1984 through 1987. Arch Ophthalmol
1992;110:838–842.
178
3. Landen D, Baker D, LaPorte R, Thoft RA. Perforating eye injury
in Allegheny County, Pennsylvania. Am J Public Health
1990;80:1120–1122.
4. Pieramici DJ, Macumber MW, Humayan MU, Marsh MJ,
de Juan E. Open-globe injury: update on types of injuries
and visual results. Ophthalmology 1996;103:1798–1803.
5. Isaac DLC, Ghanem VC, Nascimento MA, Torigoe M,
Kara-Jose N. Prognostic factors in open globe injuries.
Ophthalmologica 2003;217:431–435.
6. Tielsch JM, Parver L, Shankar B. Time trends in the incidence
of hospitalized ocular trauma. Arch Ophthalmol 1989;107:
519–523.
7. Levatin P, Prasloski PF, Collen MF. The swinging flashlight test
in multiphasic screening for eye disease. Can J Ophthalmol
1973;8:356–359.
8. Werner MS, Dana MR, Viana MAG, Shapiro M. Predictors
of occult scleral rupture. Ophthalmology 1994;101:
1941–1944.
9. Hatton MP, Thakker MM, Ray S. Orbital and adnexal trauma
associated with open globe injuries. Ophthal Plast Reconstr
Surg 2002;18:458–461.
10. Kuhn F, Morris R, Witherspoon CD, Heimann K, Jeffers JB,
Treister G. A standardized classification of ocular trauma.
Graefes Arch Clin Exp Ophthalmol 1996;234:399–403.
11. Warner MA, Caplan RA, Epstein BS, et al. Practice Guidelines
for Preoperative Fasting and the Use of Pharmacologic
Agents to Reduce the Risk of Pulmonary Aspiration:
Application to Healthy Patients Undergoing Elective
Procedures. A Report by the American Society of
Anesthesiologists: pp 1–19. Available online at: http://
www.asahq.org/publicationsAndServices/NPO.pdf
12. Ljungqvist O, Soreide E. Preoperative fasting. Br J Surg
2003;90:400–406.
13. Pandit SK, Loberg KW, Pandit UA. Toast and tea before
elective surgery? A national survey on current practice.
Anesth Analg 2000;90:1348–1351.
14. Ferrari LR, Rooney FM, Rockoff MA. Preoperative fasting
practices in pediatrics. Anesthesiology 1999;90:978–
980.
15. Benson WH, Snyder IS, Granus V, Odom JV, Macsai MS.
Tetanus prophylaxis following ocular injuries. J Emerg Med
1993;11:677–683.
16. Barr CC. Prognostic factors in corneoscleral lacerations.
Arch Ophthalmol 1983;101:919–924.
17. Scott IU, Mccabe CM, Flynn HW, et al. Local anesthesia with
intravenous sedation for surgical repair of selected open
globe injuries. Am J Ophthalmol 2002;134:707–711.
18. Lo MW, Chalfin S. Retrobulbar anesthesia for repair of
ruptured globes. Am J Ophthalmol 1997;123:833–835.

19. Narang S, Gupta V, Gupta A, Dogra MR, Pandav SS, Das S.
Role of prophylactic intravitreal antibiotics in open globe
injuries. Indian J Ophthalmol 2003;51:39–44.
20. Aguilar HE, Meredith TA, Shaarawy A, Kincaid M, Dick J.
Vitreous cavity penetration of ceftazidime after intravenous
administration. Retina 1995;15:154–159.
21. Meredith TA, Aguilar HE, Shaarawy A, Kincaid M, Dick J,
Niesman MR. Vancomycin levels in the vitreous cavity
after intravenous administration. Am J Ophthalmol
1995;119:774–778.
22. Hariprasad SM, Mieler WF, Holz ER. Vitreous and aqueous
penetration of orally administered gatifloxacin in humans.
Arch Ophthalmol 2003;121:345–350.
23. Hariprasad SM, Mieler WF, Holz ER. Vitreous penetration of
orally administered gatifloxacin in humans. Trans Am
Ophthalmol Soc 2002;100:153–159.
24. Gilbert CM, Soong HK, Hirst LW. A two-year prospective
study of penetrating ocular trauma at the Wilmer
Ophthalmological Institute. Ann Ophthalmol 1987;19:104–106.
25. Abu el-Asrar AM, al-Amro SA, al-Mosallam AA, al-Obeidan S.
Post-traumatic endophthalmitis: causative organisms and
visual outcome. Eur J Ophthalmol 1999;9:21–31.
26. Olson JC, Flynn HW, Forster RK, Culbertson WW. Results
in the treatment of post-operative endophthalmitis.
Ophthalmology 1983;90:692–699.
27. Esmali B, Elner SG, Schork A, Elner VM. Visual outcome and
ocular survival after penetrating trauma. Ophthalmology
1995;102:393–400.
28. Brinton GS, Aaberg TM, Reeser FH, Topping TM, Abrams GW.
Surgical results in ocular trauma involving the posterior
segment. Am J Ophthalmol 1982;93:271–278.
29. Reynolds DS, Flynn HW Jr. Endophthalmitis after penetrating
ocular trauma. Curr Opin Ophthalmol 1997;8:32–38.
Open globe injuries: ruptures and lacerations
30. Brinton GS, Topping TM, Hyndiuk RA, Aaberg TM, Reeser FH,
Abrams GW. Post-traumatic endophthalmitis. Arch
Ophthalmol 1984;102:547–550.
31. Affeldt JC, Flynn HW, Forster RK, Mandelbaum S, Clarkson JG,
Jarus GD. Microbial endophthalmitis resulting from ocular
trauma. Ophthalmology 1987;94:407–413.
32. Alfaro DV, Roth D, Liggett PE. Posttraumatic endophthalmitis.
Retina 1994;14:206–211.
33. Thompson WS, Rubsamen PE, Flynn HW, Schiffman J,
Cousins SW. Endophthalmitis after penetrating trauma.
Ophthalmology 1995;102:1696–1701.
34. Alexander DA, Kemp RV, Klein S, Forrester JV. Psychiatric
sequelae and psychosocial adjustment following ocular
trauma: a retrospective pilot study. Br J Ophthalmol
2001;85:560–562.
35. Vote BJ, Elder MJ. Cyanoacrylate glue for corneal perforations:
a description of a surgical technique and a review of the
literature. Clin Exp Ophthalmol 2000;28:437–442.
36. Eisner G. Eye Surgery: An Introduction to Operative
Techniques. New York: Springer-Verlag; 1990.
37. Sternberg P, de Juan E, Michels RG, Auer C. Multivariate
analysis of prognostic factors in penetrating ocular injuries.
Am J Ophthalmol 1984;98:467–472.
38. De Juan E, Sternberg P, Michels R. Penetrating ocular injuries:
types of injuries and visual results. Ophthalmology 1983;90:
1318–1322.
39. Hutton WL, Fuller DG. Factors influencing final visual
results in severely injured eyes. Am J Ophthalmol
1984;97:715–722.
40. Groessl S, Nanda SK, Mieler WF. Assault-related penetrating
ocular injury. Am J Ophthalmol 1993;116:26–33.
179

Open globe injuries:
intraocular foreign body
James T. Banta, Jeffrey K. Moore
INTRODUCTION
Penetrating ocular trauma with retained intra-
ocular foreign body (IOFB) remains one of the
most challenging and dramatic events encoun-
tered by ophthalmologists. The diagnosis requires
a detailed history and examination. Radiologic
imaging is often necessary to confi rm the diag-
nosis. Once the diagnosis is confi rmed, appropri-
ate management varies depending on the location
of the IOFB and concomitant ocular injury. Con-
sultation with a vitreoretinal specialist is recom-
mended for management of posterior segment
foreign bodies.
EPIDEMIOLOGY
Nearly 2.5 million eye injuries occur annually in
the United States.1,2 Although IOFB injuries
make up only a small overall portion of these
injuries, they contribute significantly to the cases
in which extensive surgical intervention is neces-
sary. An IOFB is present in 20–40% of penetrat-
ing ocular injuries. 3,4 The composition of the
foreign body is most often metallic, ranging in
most reports from 86% to 96%.1,3,5–8 A multi-
tude of other substances have been reported
including glass, plastic, and cilia. There is a
strong predilection for these injuries to occur in
young, male workers, particularly those ham-
mering metal on metal.8–13 In a large case series
of 297 patients with retained IOFB, 98% of
patients were male and 80% of accidents occurred
while hammering.11
12
PATHOPHYSIOLOGY
Entry into the eye by an IOFB usually occurs
because of small size, sharp edges, and rapid
velocity. This is particularly true in accidents
involving hammering metal on metal, chiseling,
or operating a metal grinder. Small sharp objects
with rapid velocity enter the eye with minimal
disruption of surrounding tissues. Oftentimes,
small corneal or corneoscleral entry wounds will
be self-sealing.
Conversely, large IOFB, particularly those
without sharp edges (e.g. BB), require a tremen-
dous amount of force to enter the eye. The con-
cussive effect on the eye leads to tremendous
concomitant ocular disruption and poor visual
prognoses.
EVALUATION
A high index of suspicion is vital when consider-
ing an IOFB and history is a critical component
of the ocular trauma workup. Several important
questions need to be posed:
1. When did the injury occur?
2. What was the mechanism of injury?
3. Was eye protection in place at the time of the
accident?
4. In an industrial accident, what type of mate-
rial was being worked with (e.g. iron, glass,
wood, etc.)?
The clinical history will raise or lower the sus-
picion of IOFB and will assist in guiding the
subsequent examination and ancillary studies.
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-
cian experienced in ocular ultrasonography.
Ultrasound biomicroscopy, although not always
readily available, is a useful tool for detecting
occult foreign bodies of the anterior segment.20
Magnetic resonance imaging (MRI) is not
appropriate for imaging and localizing IOFBs.
The movement of ferromagnetic foreign bodies
can induce significant migration21 and secondary
local ocular damage22 or even blindness.23
All radiologic studies should be personally
reviewed with a radiologist.
TREATMENT
The management of an IOFB begins even before
the diagnosis is confi rmed. Avoiding unnecessary
and extensive manipulation of an injured eye is
always important. Placement of a protective
184
Figure 12.4 B-scan ultrasound of two different patients
demonstrates an intraocular foreign body within the
vitreous cavity (A) and within the substance of the
retina (B). Note the acoustic shadowing posterior to
both foreign bodies.
shield (e.g. Fox shield) and encouraging the
patient not to touch the eye are equally vital.
Four primary goals are present when confront-
ing the IOFB patient:
1. preservation of vision
2. prevention of infection
3. restoration of normal eye architecture
4. prevention of long-term sequelae.
Tetanus prophylaxis is given if not current. Most
surgeons prefer to begin prophylactic systemic
antibiotics immediately. In the acute setting,
they can be administered prior to and during
ancillary testing. Antibiotic selection should be

Figure 12.5 Intraocular air masquerading as IOFB. An
experienced ultrasound technician is vital in properly
utilizing and interpreting ocular ultrasonography.
directed towards the commonly encountered
organisms found with open globes. Antibiotic
use is controversial and is covered later in this
chapter.
The fi nal resting position of the IOFB and the
degree of concomitant injury determine the
approach and extent of surgical intervention.
Anterior chamber, intralenticular, and posterior
chamber foreign bodies raise different surgical
challenges and management considerations.
Anterior chamber foreign bodies
One-quarter to one-third of IOFBs will remain
anterior to the posterior lens capsule11 (Figure
12.6) and are technically less difficult to remove
than posteriorly situated foreign bodies. Entry
wounds through the cornea or limbus are cleared
of any prolapsed iris, always favoring reposition
of viable uvea if feasible. Closure of the wound
with 10-0 nylon sutures as described in the pre-
vious chapter is then performed. Once the ante-
rior chamber is closed, a limbal paracentesis or
a beveled clear corneal incision is created several
clock hours away from the foreign body. Visco-
elastic is used to maintain the anterior chamber
depth and protect the corneal endothelium and
Open globe injuries: intraocular foreign body
Figure 12.6 Anterior chamber foreign bodies are
uncommon. Cilia as an anterior chamber foreign body
is exquisitely rare.
anterior lens capsule. Viscoelastic can also be
used to manipulate and move small foreign
bodies, providing for safe and efficient removal.
If visualization is problematic, a surgical gonios-
copy lens (e.g. Koeppe lens) is utilized to directly
visualize the foreign body to lessen the risk of
iris damage with blind attempts at grasping the
IOFB. Once the foreign body is localized, it is
grasped under direct visualization with forceps
and removed through the limbal incision, enlarg-
ing as necessary. Bimanual techniques are some-
times needed to extract a foreign body imbedded
in the iris. A metallic foreign body can some-
Included
times be removed with an intraocular magnet. on DVD
Intralenticular foreign bodies
Intralenticular foreign bodies (ILFB) are not
commonly encountered, accounting for only 7–
10% of all intraocular foreign bodies. Most intra-
lenticular foreign bodies are removed at the
time of injury in hopes of preventing infection,
inflammation, secondary cataract, or siderosis
(Figure 12.7). Lens capsule breach significantly
increases the risk of post-traumatic endophthal-
mitis.24 Surgical removal of an intralenticular
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
phacoemulsification can typically be performed
with forceps removal of the foreign body.25 Small
intraocular foreign bodies may resorb spontane-
ously, become encapsulated, lose magnetic prop-
erties and become radiolucent to X-rays. Such
intralenticular foreign bodies can be tolerated for
years without surgical intervention.26 Case
reports in the literature include an 18-year-old
male with an intralenticular foreign body and
20/20 visual acuity 13 years after injury,27 a 61-
year-old male with 20/25 vision 23 years follow-
ing injury,28 and a 58-year-old male who retained
good vision without siderosis for 40 years.29 It is
thought that small wounds of the anterior lens
capsule can self-seal and re-epithelialize allow-
ing the foreign body to remain sequestered.
Thus, if the risk of infection is small, inflamma-
tion is limited, ILFB composition is acceptable,
and cataract formation is not visually significant,
cautious observation is a viable option for the
ILFB. However, if the ILFB is ferromagnetic,
serial electroretinograms (ERG) should be per-
formed every 2–3 months to monitor for sidero-
sis bulbi. 30,31 This feared sequela of a ferromagnetic
intralenticular foreign body is characterized by
iris heterochromia, mydriasis, cataract, chronic
uveitis, secondary glaucoma, retinal pigmentary
degeneration, and optic disc swelling. ERG
changes noted in siderosis include a large a wave
and normal b wave early in the course with
diminished (or possibly extinguished) b wave
amplitude later in the course. Siderosis bulbi is
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
complaining of a foreign body sensation in the left
eye. A piece of metal had hit him in the face 3 days
prior to presentation. He had been hammering
metal on metal without protective eyewear. His
initial examination was significant for a visual acuity
of 20/20, a normal intraocular pressure, a self-sealed
corneal laceration, minimal cell and flare, an anterior
capsular disruption (white arrow, A), and an intralen-
ticular foreign body. The anterior chamber was deep
and the corneal wound was negative by Seidel
testing. No foreign bodies were noted in the vitre-
ous. An ultrasound and an orbital CT scan were sig-
A B
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on DVD
C D
Open globe injuries: intraocular foreign body
nificant for an isolated, metallic, intralenticular foreign
body (B). Given the patient’s excellent vision and lack
of infection, siderosis bulbi, or cataract, observation
was chosen. He received oral antibiotics, topical ste-
roids and topical antibiotics initially and was then
followed with serial examinations. He was lost to
follow-up but returned 6 weeks after his injury for a
baseline ERG. The ERG revealed a large a wave con-
sistent with early siderosis. The rod and cone ERG
responses were also increased in amplitude and pro-
longed. In addition, the patient now complained of
decreasing vision and was noted to have developed
a traumatic subcapsular cataract (C). Given his ERG
187
 Ocular trauma
Case report: intralenticular foreign body (cont’d)
findings and the developing cataract, he underwent
removal of the metallic foreign body with forceps
(D), phacoemulsification of the crystalline lens,
and implantation of a posterior chamber intraocular
Posterior segment foreign bodies
Posterior segment foreign bodies represent the
vast majority of IOFB and necessitate consulta-
tion with a vitreoretinal specialist for defi nitive
management. Surgical intervention of posterior
segment IOFB has changed significantly with
the advent of closed vitrectomy. Although
several studies have shown no difference in visual
outcome using an external electromagnet (EEM)
versus pars plana vitrectomy (PPV), 32,33 refi ned
PPV techniques allow excellent control of for-
eign bodies and have shown a propensity for
improved visual outcomes and diminished rates
of endophthalmitis.34
CASE EXAMPLES
Case report: intraocular foreign body (Figure 12.9)
A 30-year-old male was hammering metal on metal
when he felt something strike his left eye. He had
immediate mild pain and mildly decreased vision. He
presented to the emergency room for treatment. On
A B
188
lens. The patient had a final visual acuity of 20/20
and tolerated the procedure well without further
complications.
Timing of IOFB removal remains controversial.
A posterior segment IOFB is generally considered
a surgical emergency. Immediate removal is thought
to reduce the incidence of endophthalmitis. The
removal of posterior intraocular foreign bodies
often requires a broad range of vitreoretinal tech-
niques. Typical steps include stabilization of the
entry wound, pars plana lens extraction, stabiliza-
tion and repair of the retina, and forceps or mag-
netic removal of the foreign body. Scleral buckling
is often advantageous as these cases are at a high
risk for the development of proliferative vitreore-
tinopathy (PVR). While the use of intravitreal
antibiotics is controversial, the authors advocate
their use when conditions permit.
examination, visual acuity was 20/20 OD and 20/70
OS. There was no relative afferent pupillary defect
and intraocular pressures were 22 and 23 in the right
and left eye, respectively. Slit lamp examination of

Case report: intraocular foreign body (cont’d)
the anterior segment was notable for the absence of
obvious corneal lacerations or transillumination
defects of the iris or lens capsule. A suspicious area
was seen in the temporal sclera but was obscured
by focal conjunctival edema and chemosis. A small
amount of vitreous hemorrhage was seen on the
surface of the posterior capsule (A). Dilated fundus
exam through a mild amount of vitreous hemor-
rhage revealed a triangular-shaped metallic frag-
ment embedded in the retina superior and temporal
C D
COMPLICATIONS AND OUTCOMES
Endophthalmitis is a devastating, yet common
complication of IOFB. The reported incidence of
endophthalmitis following an IOFB varies widely,
occurring in 7% 35 to 48% 36 of eyes. The risk of
endophthalmitis is related to the mode of injury
and the ‘dirtiness’ of the IOFB. Intraocular
organic material and grossly dirty metallic objects
have a very high risk of subsequent endophthal-
mitis. In cases where the object is felt to be
‘clean,’ the use of prophylactic antibiotics remains
controversial. Systemic antibiotics are also rou-
tinely used, although not fully supported in the
literature. When selecting systemic antibiotics, a
specific goal of achieving adequate vitreous levels
is vital. Fluoroquinolones and third generation
Open globe injuries: intraocular foreign body
to the fovea just inferior to the superotemporal vas-
cular arcade (B). B-scan ultrasound revealed only the
single IOFB visualized on dilated fundus exam (C).
The eye was covered with a shield and the patient
was admitted for I.V. antibiotics and surgery. A pars
plana vitrectomy was performed and the IOFB was
removed using an intraocular magnet. Three weeks
following surgery, the retina was attached and the
impact site was clearly visible (D). Visual acuity was
20/200.
cephalosporins demonstrate therapeutic concen-
trations in the vitreous. Gatifloxacin has been
shown to achieve excellent therapeutic levels in
the vitreous when administered systemically. 37
Vancomycin has also been shown to reach ade-
quate levels in eyes that are inflamed or in the
postoperative period. 38 A typical combination
regimen of an intravenous third generation
cephalosporin (typically ceftazidime) and vanco-
mycin is generally given while the patient is hos-
pitalized. These can be followed by an outpatient
course of an oral fluoroquinolone. Intraocular
antibiotics may also be administered at the time
of surgery. Vancomycin (1 mg in 0.1 cc) and
ceftazidime (2.25 mg in 0.1 cc) are well
tolerated intravitreally and are commonly admin-
istered prophylactically at the time of IOFB
189
 Ocular trauma
removal. Broad-spectrum topical antibiotics are
recommended postoperatively.
Beyond the direct injury inflicted by an IOFB,
chemical toxicity is often a prime concern depend-
ing on the foreign body’s composition. Copper
foreign bodies are of paramount concern given the
risk of acute chalcosis: a fulminate, sterile inflam-
matory reaction that mimics infectious endophthal-
mitis. A more benign form of chronic chalcosis can
also occur later in the disease process, typically
causing a ‘sunflower’ cataract and a green discolor-
ation of the iris. Ferromagnetic foreign bodies can
cause siderosis, a chronic deposition of iron that
leads to iris heterochromia, cataract, and progres-
sive pigmentary retinal degeneration. Siderosis and
chalcosis are discussed further in Chapter 13.
Concomitant injury to the eye is a common cause
of poor visual outcome. Central corneal wounds
may necessitate delayed penetrating keratoplasty.
Secondary glaucoma as well as iris and ciliary
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
eye protection when he felt something strike his
right eye. He reported immediate pain and decreased
vision in the right eye. Initial visual acuity was 20/70
and 20/20 in the right and left eye respectively.
Examination of the left eye was entirely normal.
Intraocular pressure measurement was deferred until
Included
on DVD a screening slit lamp examination was performed.
An intraocular foreign body was readily visible (A).
The foreign body entered the inferotemporal cornea,
pierced the inferotemporal iris, entered the retina
just posterior to the pars plana, and came to rest in
a subretinal location at the equator. A surprising lack
of hemorrhage allowed an excellent view of the pos-
terior segment. The patient was admitted and given
I.V. antibiotics, tetanus prophylaxis, and topical anti-
biotics. Surgery was undertaken several hours later
190
macular scarring, proliferative vitreoretinopathy
and traumatic optic neuropathy are common
posterior segment causes of poor outcomes.
Multiple reconstructive surgeries may be needed.
Visual acuity outcomes following an IOFB vary
widely in published reports, but there is a clear
trend towards improved visual outcomes with
modern surgical techniques, improved localiza-
tion with computed tomography, and improved
antibiotic selection and usage in the last decade.
Multiple variables are associated with a poor
visual prognosis. These include poor preoperative
visual acuity, 39 relative afferent pupillary defect, 8
and a large foreign body.4,6 Good visual acuity
results are often associated with an anterior loca-
tion of the foreign body (anterior to the posterior
lens capsule) and minimal surrounding tissue
injury (vitreous hemorrhage, retinal detachment,
etc.). A fi nal visual acuity of ≥ 20/40 is seen in
approximately 30–70% of cases.
at which time a thorough pars plana vitrectomy was
performed to remove any vitreous traction. The
large foreign body was then carefully removed using
forceps (B) and the corneal wound was closed with
10-0 nylon sutures. Prophylactic endolaser and cryo-
therapy were placed in the area of retinal disruption
(C). Gross examination of the foreign body revealed
thin gauge wire approximately 2 cm in length (D).
Postoperatively, the patient did well. A small corneal
scar and early posterior subcapsular cataract are
seen at a follow-up visit 2 months after surgery (E,
just prior to suture removal). The retina remained flat
with extensive chorioretinal scarring in the area of
retinal laser (F; white arrow denotes the anterior
extent of the initial IOFB position). Visual acuity was
20/30 5 months after surgery.
 Open globe injuries: intraocular foreign body

Case report: intraocular foreign body (cont’d)

A B

C D

E F

191
 Ocular trauma
SUMMARY
1. IOFB is a harrowing diagnosis for the patient
and ophthalmologist.
2. IOFB most commonly occurs in young men
hammering metal on metal in the absence of
protective eyewear.
3. Careful history taking and examination are a
vital portion of the workup and can secure the
diagnosis in some instances, but computed
tomography or ultrasound are often necessary
to confi rm the diagnosis and rule out multiple
foreign bodies.
4. Surgical removal of an IOFB is determined by
the fi nal resting place of the foreign body as
well as concomitant ocular injuries.
5. Metallic intralenticular foreign bodies must
be followed serially with electrophysiologic
testing if observation is elected.
6. Posterior segment IOFB requires consultation
with a vitreoretinal specialist for defi nitive
management.
REFERENCES
1. Feist RM, Farber MD. Ocular trauma epidemiology. Arch
Ophthalmol 1989;107:503–504.
2. Tielsch JM, Parver L, Shankar B. Time trends in the incidence
of hospitalized ocular trauma. Arch Ophthalmol
1989;107:519–523.
3. Shock JP, Adams D. Long term visual acuity results after
penetrating and perforating ocular injuries. Am J Ophthalmol
1985;100(5):714–718.
4. Thompson JT, Parver LM, Enger CL, et al. Infectious
endophthalmitis after penetrating injury with retained
intraocular foreign bodies. Ophthalmology 1993;100:
1468–1474.
5. Abu El-Asrar AM, Al-Amro SA, Khan NM, Kangave D. Visual
outcome and prognostic factors after vitrectomy for
posterior segment foreign bodies. Eur J Ophthalmol
2000;10:304–311.
6. Coleman DJ, Lucas BC, Rondeau MJ, Chang S. Management
of intraocular foreign bodies. Ophthalmology 1987;94:
1647–1653.
192
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.
8. De Souza S, Howcroft MJ. Management of posterior segment
intraocular foreign bodies: 14 years’ experience. Can J
Ophthalmol 1999;34:23–29.
9. Dannenberg AL, Parver LM, Brechner RJ, Khoo L. Penetrating
eye injuries in the workplace: the National Eye Trauma System
Registry. Arch Ophthalmol 1992;110:843–848.
10. Armstrong MFJ. A review of intraocular foreign body injuries
and complications in N. Ireland from 1978–1986. International
Ophthalmology 1988;12:113–117.
11. Behrens-Baumann W, Praetorius G. Intraocular foreign bodies,
297 consecutive cases. Ophthalmologica 1989;198:84–88.
12. Punnonen E, Laatikainen L. Prognosis of perforating eye
injuries with intraocular foreign bodies. Acta Ophthalmol
1989;67:483–491.
13. Greven CM, Engelbrecht NE, Slusher MM, Nagy SS. Intraocular
foreign bodies: management, prognostic factors, and visual
outcomes. Ophthalmology 2000;107:608–612.
14. Bryden FM, Pyott AA, Bailey M, McGhee CNJ. Real time
ultrasound in the assessment of intraocular foreign body.
Eye 1990;4:727–731.
15. Bray LC, Griffiths PG. The value of plain radiography in
suspected intraocular foreign body. Eye 1991;5:751–754.
16. Dass AB, Ferrone PJ, Chu YR, et al. Sensitivity of spiral
computed tomography scanning for detecting intraocular
foreign bodies. Ophthalmology 2001;108:2326–2328.
17. Chacko JG, Figueroa RE, Johnson MH, et al. Detection and
localization of steel intraocular foreign bodies using
computed tomography: a comparison of helical and
conventional axial scanning. Ophthalmol 1997;104:319–323.
18. Lakits A, Prokesch R, Scholda C, et al. Multiplanar imaging
in the preoperative assessment of metallic intraocular
foreign bodies, helical computed tomography versus
conventional computed tomography. Ophthalmology
1998;105:1969–1985.
19. Zacks DN, Hart L, Young LGY. Ultrasonography in the
traumatized eye: intraocular foreign body versus artifact.
Int Ophthalmol Clin 2002;42(3):121–128.
20. Deramo VA, Shah GK, Baumal CR, et al. Ultrasound
biomicroscopy as a tool for detecting and localizing occult
foreign bodies after ocular trauma. Ophthalmology
1999;106:301–305.
21. Gunenc U, Maden A, Kaynak S, Pirnar T. Magnetic resonance
imaging and computed tomography in the detection and
localization of intraocular foreign bodies. Doc Opthalmol
1992;81:369–378.

22. Ta CN, Bowman RW. Hyphema caused by a metallic
intraocular foreign body during magnetic resonance
imaging. Am J Ophthalmol 2000;129:533–534.
23. Kelly WM, Paglen PG, Pearson JA San Diego AG, Soloman MA.
Ferromagnetism of intraocular foreign body causes unilateral
blindness after MR study. Am J Neuroradiology 1986;7:
243–245.
24. Essex RW, Yi Q, Charles PG, Allen PJ. Post-traumatic
endophthalmitis. Ophthalmology 2004;111:2015–2022.
25. Arora R, Sanga L, Kumar M, Taneja M. Intralenticular foreign
bodies: report of eight cases and review of management.
Indian J Ophthalmol 2000;48:119–122.
26. Lee LL, Briner AM. Intralenticular metallic foreign body.
Australian NZ J Ophthalmol 1996;24:361–363.
27. Keeney AH. Intralenticular foreign bodies. Arch Ophthalmol
1971;86(5):499–501.
28. Macken PL, Boyd SR, Feldman F. Intralenticular foreign bodies:
case reports and surgical review. Ophthalmic Surg 1995;26(3):
250–252.
29. Cazabon S, Dabbs TR. Intralenticular metallic foreign body.
J Cataract Refract Surg 2002;28:2233–2234.
30. O’Duffy D, Salmon JF. Siderosis bulbi resulting from
an intralenticular foreign body. Am J Ophthalmol
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.
Open globe injuries: intraocular foreign body
32. Chow DR, Garretson BR, Kuczynski B, et al. External versus
internal approach to the removal of metallic intraocular
foreign bodies. Retina 2000;20:364–369.
33. Pavlovic S, Schmidt KG, Tomic Z, et al. Management of intra-
ocular foreign bodies and endophthalmitits. Ophthalmology
1990;97:1532–1538.
34. Mester V, Kuhn F. Ferrous intraocular foreign bodies retained
in the posterior segment: management options and results.
Int Ophthalmol 1998;22:355–62.
35. Mieler WF, Ellis MK, Williams DF, Han DP. Retained intraocular
foreign bodies and endophthalmitis. Ophthalmology
1990;97:1532–1538.
36. Kazokoglu H, Saatci O. Intraocular foreign bodies: results of 27
cases. Ann Ophthalmol 1990;22:373–376.
37. Hariprasad SM, Mieler WF, Holz ER. Vitreous and aqueous
penetration of orally administered gatifloxacin in humans.
Arch Ophthalmol 2003;121:345–350.
38. Meredith TA, Aguilar HE, Shaarawy A, et al. Vancomycin levels
in the vitreous cavity after intravenous administration. Am J
Ophthalmol 1995;119:774–778.
39. Jonas JB, Knorr HL, Budde WM. Prognostic factors in ocular
injuries caused by intraocular or retrobulbar foreign bodies.
Ophthalmology 2000;107:823–828.
193

Delayed complications of
ocular injury
James T. Banta
INTRODUCTION
Ocular trauma, as illustrated in the previous
chapters, is a diverse spectrum of disease pro-
cesses affecting all portions of the eye. Most
injuries lead to a rapid onset of symptoms and
diagnostic dilemmas are fairly unusual once
a familiarity with the various conditions is
obtained. It is important to note, however, that
multiple pathologic conditions do not present
acutely. Many can be delayed by days (traumatic
iritis) to months (traumatic cataract) to years
(angle recession glaucoma).
In this chapter, we will describe ocular com-
plications of ocular trauma that are not necessar-
ily present on initial examination and which
require prolonged follow-up. These entities
range from self-limited to vision-threatening and
require diligence on the part of the physician to
correctly diagnose and treat. Diagnoses covered
in prior chapters will be mentioned briefly and
cross-referenced to the chapter containing a
detailed description.
TRAUMATIC IRITIS
Traumatic iritis is a very common condition
that typically occurs hours to days after a contu-
sive injury to the eye. Typically, an antecedent
history of ocular injury, often mild, is elucidated.
Common presenting symptoms include photo-
phobia, blurry vision, and pain. Examination
fi ndings include conjunctival injection and an
anterior chamber cellular response. Treatment
involves cycloplegia plus or minus steroid drops.
Traumatic iritis is covered in detail in Chapter 6.
13
TRAUMATIC CATARACT
A cataract may develop any time following a
traumatic injury. The timeframe depends pri-
marily on the mechanism of trauma. Direct
injury to the lens capsule often leads to immedi-
ate formation of cataract, whereas mature cata-
racts can present decades after a contusive
injury. It is important to elucidate a history of
trauma when planning cataract surgery since
antecedent trauma predisposes to zonular injury
and intraoperative complications. Symptoms
are usually limited to diminished vision. Signs
include phacodonesis, iridodonesis, lens sublux-
ation/dislocation, vitreous prolapse or a monoc-
ular mature cataract. Traumatic cataract is
covered in detail in Chapter 7.
DELAYED TRAUMA-RELATED
GLAUCOMA
Glaucoma can occur via multiple mechanisms
following ocular trauma. Some forms of glau-
coma may occur months to years following the
inciting injury, re-emphasizing the importance
of appropriate long-term follow-up after ocular
trauma.
Angle recession glaucoma
Contusive ocular injury can lead to a rapid equa-
torial expansion of the eye. One manifestation
of this injury type is a traumatic separation of
the longitudinal and circular fibers of the ciliary
body. Angle recession has a characteristic gonio-
scopic appearance and should be specifically
ruled out after any substantial contusive eye
195
 Ocular trauma
injury. Angle recession is covered in detail in
Chapter 6.
Vitreous hemorrhage-induced glaucoma
Following traumatic vitreous hemorrhage, par-
ticularly in patients with disruption of the
anterior hyaloid face and zonular apparatus, red
blood cells (RBC) and RBC breakdown products
can freely fi lter into the anterior chamber and
obstruct the trabecular meshwork. Three dis-
tinct entities have been described depending on
the level of RBC breakdown that has occurred:
1. Ghost cell glaucoma. RBCs undergo a step-
wise degradation as they remain in the vitre-
ous cavity. Dehemoglobinized cells are more
rigid and spherical than regular RBCs and
mechanically block the trabecular meshwork
when introduced to the anterior chamber.
Khaki-colored cells can often be seen circulat-
ing in the anterior chamber and sometimes
layer out as a pseudo-hypopyon.
2. Hemolytic glaucoma. Further degradation of
RBCs leaves cellular debris, free hemoglobin,
and macrophages laden with breakdown prod-
ucts to mechanically obstruct the trabecular
meshwork.
3. Hemosiderotic glaucoma. Iron freed during
the breakdown of RBCs can be toxic to the
endothelium lining the trabecular meshwork
months to years after vitreous hemorrhage.
This toxicity can lead to sclerosis and mal-
function of aqueous egress from the eye with
subsequently elevated intraocular pressure.
Treatment for each of these forms of glaucoma
begins with standard medical therapy to slow
aqueous production and facilitate outflow. If
these measures are unsuccessful, as they
frequently are, surgical intervention with pars
plana vitrectomy and anterior chamber washout
is frequently necessary. The diagnosis of these
very rare forms of glaucoma requires a high
196
degree of clinical suspicion. A thorough history
is of the utmost importance since the inciting
injury can be fairly remote.
Lens-induced glaucoma
Trauma to the crystalline lens can cause glau-
coma by a variety of open and closed angle
mechanisms. The primary clinical entities
include:
1. Phacolytic glaucoma. Elevated IOP caused by
leakage of lens proteins through the intact
capsule of a hypermature cataract.
2. Phacomorphic glaucoma. Elevated IOP caused
by angle closure induced by a mature or
rapidly evolving traumatic cataract.
3. Lens particle glaucoma. Elevated IOP caused
by mechanical blockage of the trabecular
meshwork by liberated lens particles following
trauma.
4. Phacoanaphylactic glaucoma. Elevated IOP
caused by profound granulomatous inflamma-
tory response to liberated lens particles.
Lens-induced glaucoma is covered in detail in
Chapter 7.
RETINAL DETACHMENT
Retinal detachment is the fi nal common pathway
for an array of trauma-induced peripheral retinal
injuries. Vitreoretinal attachments are much
stronger in young patients, the demographic
representing most ocular traumas. When
these attachments are traumatically disrupted, a
variety of injuries occur including:
1. retinal dialysis
2. giant retinal tear
3. horseshoe tear
4. pars plana tear
5. necrotic retinal break
6. vitreous base avulsion.
 Delayed complications of ocular injury

Careful peripheral retinal examination is vital
following ocular injury. If a view to the posterior
segment is obstructed or scleral depression is not
possible due to concomitant injuries, ultrasound
can be used to monitor the status of the retina.
Traumatic retinal detachment is covered in
detail in Chapter 8.
METALLOSIS BULBI
Retained intraocular foreign body (IOFB) occurs
in 5–40% of all open globe injuries. Careful
clinical evaluation is critical for the diagnosis of
an intraocular foreign body given its propensity
for infection and toxicity. Most IOFB are metal-
lic and occur in young males hammering metal
on metal or grinding. The composition of an
IOFB determines its toxicity to the eye (Table
13.1). Precious metals such as gold and platinum
are well tolerated in the posterior segment.
Foreign bodies containing iron or copper are
common and can lead to severe ocular toxicity
and potential blindness.

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

198
 Delayed complications of ocular injury

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

CASE EXAMPLES

Case report: siderosis secondary to IOFB (Figure 13.3)

A 24-year-old male was hammering metal on metal
without eye protection when he felt something
Included
on DVD
strike his left eye. Despite a foreign body sensation
and decreased vision, he did not seek medical
attention. Two months later, he presented with a
progressive decline in vision of the left eye. Visual
acuity was 20/200 OS with an afferent pupillary
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-
ocular foreign body in the superonasal periphery
surrounded by extensive pigmentary alterations (A).
B-scan ultrasound revealed only the single intra-
ocular foreign body (B). An electroretinogram was
obtained and revealed severe, diffuse depression of
both photopic and scotopic examinations (C). The
Chalcosis
Retained copper-containing IOFB is an uncom-
mon clinical entity. Common sources of injury
with copper include explosions (bullet casings,
mines, or grenades) and industrial work with
copper alloys. The most common copper
alloys are brass and bronze, both of which
typically contain less than 85% copper. Intraocu-
lar copper foreign bodies show a wide range
of fi ndings ranging from an acute fulminant,
endophthalmitis-like picture to an indolent
deposition of copper in various ocular basement
membranes.
Acute chalcosis is typically seen with foreign
bodies containing more than 85% copper.6 It is
characterized by a profound inflammatory
response that leads to destruction of intraocular
contents within a short period of time. The only
treatment is expedient removal of the offending
foreign body and the outcomes are typically
poor. It is important to note that this reaction
does not occur universally, even with pure copper
foreign bodies.7
Although variable, classic teaching states that
chronic chalcosis occurs with IOFB containing
less than 85% copper.6 The inflammatory
response is less severe and may be minimal. The
primary mechanism of toxicity is deposition of
copper in various membranes within the eye.
Classic ocular fi ndings include:
Delayed complications of ocular injury
diagnosis of siderosis bulbi was made. The patient
underwent uneventful par plana vitrectomy and
removal of the intraocular foreign body. (D) The
foreign body was removed by intraocular forceps
through a sclerotomy incision. Visual acuity remained
20/200 postoperatively.
1. sunflower cataract
2. iris heterochromia (typically a greenish dis-
coloration of the affected iris)
3. deposits on the retinal surface
4. free copper particles in the aqueous or
vitreous
5. Descemet’s membrane deposits forming a
peripheral corneal ring (Kayser–Fleischer).
The clinical course of chronic chalcosis is vari-
able, but typically indolent. ERG changes are
typically absent or minimal.8 Removal of the
foreign body should be undertaken if visual com-
promise is evident.
SYMPATHETIC OPHTHALMIA
Sympathetic ophthalmia is one of the least
common yet most feared complications of ocular
trauma. It is a bilateral granulomatous uveitis
that occurs after injury to the eye, most com-
monly following open globe injury but also
known to occur after intraocular surgery. 9 The
pathophysiology of the disease process, particu-
larly the antigen that elicits the inflammation, is
debated; but it appears that upon traumatic
injury, uveal antigens are exposed in a manner
that elicits a delayed autoimmune response.
The exciting, or injured eye, becomes inflamed as
does the sympathizing, or previously normal, eye.
A genetic predisposition may be a factor as indi-
201
 Ocular trauma
cated by the increased prevalence of HLA-A11
in sympathetic ophthalmia patients.10
Sympathetic ophthalmia is rare. The incidence
following open globe injury is approximately
0.2%11 to 0.5%.12 The time to onset following
injury is highly variable, typically ranging
from 2 weeks to 6 months with most cases
presenting within 3 months of injury. However,
it has been reported to occur as early as 10 days
and as late as many decades following the
inciting event.
The clinical onset is often insidious over days
to weeks. Mild, vague complaints are often
encountered early in the disease course. Mild
pain, photophobia, and mildly decreased vision
are common presenting symptoms. The symp-
toms predominate in the sympathizing eye since
the exciting eye often has poor vision and mild,
chronic discomfort. This reinforces the need for
careful examination of the uninjured eye follow-
ing an open globe injury, particularly if the
injured eye has protracted inflammation and
pain following surgical repair.
The clinical appearance of sympathetic oph-
thalmia is variable, but typically involves a granu-
lomatous panuveitis with a prominent vitritis and
characteristic changes of the posterior pole.
Mutton-fat keratic precipitates are often seen on
the corneal endothelial surface in the active phase
of the disease. The choroidal lesions are often
multifocal, placoid, and cream-colored. The cho-
roidal lesions correspond to Dalen–Fuchs nodules,
a histologic diagnosis. Optic nerve hyperemia
and swelling are sometimes present. Fluorescein
angiography reveals multiple hyperfluorescent
sites that leak late in the angiogram.
Treatment of sympathetic ophthalmia can be
broken up into preventative and active treatment
202
strategies. Enucleation of a severely injured eye
is thought to prevent sympathetic ophthalmia if
performed within 10–14 days of injury. However,
with current medical and surgical care, improved
visual outcomes are being seen following severe
ocular trauma. Enucleation is typically reserved
for eyes with no hope of visual recovery and
prominent intraocular disorganization. A candid
discussion with the patient regarding the risks of
sympathetic ophthalmia is mandatory if enucle-
ation is being considered following open globe
repair.
Once active sympathetic ophthalmia has been
diagnosed, treatment consists primarily of immu-
nosuppressive agents. The use of enucleation to
remove the exciting eye is controversial and
unlikely of any benefit.13 In some circumstances,
after the disease has progressed, the exciting eye
can maintain better visual acuity than the sym-
pathizing eye. Current medical regimens rely
heavily on steroids in high doses with long,
gradual tapers. Steroid sparing agents such as
cyclosporine, azathioprine, chlorambucil, and
methotrexate have all been used with success.
Although the exact regimen is controversial,
aggressive therapy in a timely manner is vital to
clinical success. Long-term follow-up is required
as long periods of remission may punctuate epi-
sodes of activity.
Outcomes in sympathetic ophthalmia prior to
the routine use of high dose steroids were uni-
formly poor. Refi nements in medical therapy
have improved the visual outcomes significantly.
A review of 32 sympathetic ophthalmia cases
treated with systemic steroids showed 50%
recovered vision of 20/40 or better; however,
31% had a fi nal visual acuity less than
20/200.14

CASE EXAMPLES
Case report: sympathetic ophthalmia (Figure 13.4)
A 33-year-old female was forcefully struck in the right
eye with a fist and experienced immediate and pro-
found loss of vision. She was evaluated by an oph-
thalmologist who was suspicious for a ruptured
globe. The patient was taken to the operating room
and a full-thickness 8 mm scleral wound was closed
uneventfully. The patient failed to return for follow-
up. One month after the surgical repair, the patient
presented to our ocular emergency room with com-
plaints of profound decreased vision and pain for 3
days in the left eye. Ophthalmic examination revealed
a visual acuity of light perception in the right eye and
20/200 in the left eye. Slit lamp examination of the
right eye revealed a shallow but formed anterior
chamber with a small amount of residual hyphema
and a dense cataract precluding a view of the pos-
terior pole (A). Slit lamp examination of the left eye
A B
C D
Delayed complications of ocular injury
revealed keratic precipitates, anterior chamber cell
and flare, and 360 degrees of posterior synechiae (B).
Dilated fundus examination of the left eye revealed
optic nerve swelling and hyperemia. Multifocal
cream-colored choroidal lesions and serous retinal
detachments were present throughout the posterior
pole (C). Ocular coherence tomography further
delineated the multifocal serous detachments (D).
The patient was admitted on multiple occasions for
intravenous steroids and was discharged on oral ste-
roids. Due to a poor social situation and struggles
with drug dependence, the patient failed to return
for most of her follow-up appointments and dem-
onstrated poor compliance throughout her treat-
ment course. One year after her initial presentation,
vision remained hand motions in the right eye and
20/200 in the left eye.
203
 Ocular trauma
CHOROIDAL NEOVASCULARIZATION
ASSOCIATED WITH CHOROIDAL
RUPTURE
Choroidal ruptures occur after contusive trauma
and appear as curvilinear, crescent-shaped areas
concentric to the optic disc. The major cause of
poor vision resulting from choroidal rupture,
second to a rupture involving the fovea, is late
development of a choroidal neovascular mem-
brane (CNVM). Metamorphopsia and decreased
vision typically occur if the CNVM occurs
within the macula. Clinical examination often
reveals a greenish-gray subretinal lesion that may
be associated with hemorrhage or subretinal
fluid. Fluorescein angiography is used to confi rm
the diagnosis.
CNVM associated with choroidal rupture is
covered in detail in Chapter 8.
TRAUMATIC ENDOPHTHALMITIS
Traumatic endophthalmitis is a feared complica-
tion of open globe injury. The incidence of
this potentially devastating complication ranges
widely in published reports. In years past,
reported rates have been as high as 30% follow-
ing open globe injury.15 However, more recent
studies report rates less than 10%, typically 4–
7%.16–18 The presence of an intraocular foreign
body increases the rate two- to threefold.
Risk factors for developing endophthalmitis
following open globe injury include:
1. intraocular foreign body17
2. violation of lens capsule17–19
3. contaminated wound17
4. delay in primary repair.7
Most patients with traumatic endophthalmitis
present with increasing eye pain following open
globe repair. The diagnosis is often difficult
owing to the extensive inflammation and intra-
204
ocular disruption imparted by the inciting injury
and subsequent surgical repair. A high index of
suspicion and a low threshold for intervention
are necessary. The presence of a hypopyon and
increasing membranous vitreous opacities (by
clinical examination or ultrasound if posterior
viewing is compromised) are classic fi ndings of
endophthalmitis and should prompt emergent
treatment.
The diagnosis of endophthalmitis is clinical, as
cultures of intraocular contents can be negative.
However, it is vital to obtain cultures and sensi-
tivities to further guide antibiotic choices and
identify potential patterns of emerging antibiotic
resistance. The spectrum of isolated organisms
following an open globe injury is unique. A
particularly high incidence of Bacillus species
and polymicrobial infections are encountered.
Gram positive organisms make up a majority of
infections20–22 with Staphylococcus epidermidis,
Bacillus cereus, and Streptococcus species being
the most common gram positive isolates.22 Gram
negative organisms (particularly Pseudomonas
species) and fi lamentous fungi are seen with less
frequency. Bacillus species have a particularly
fulminate course with rapid onset and a dismal
visual prognosis and should be suspected if endo-
phthalmitis develops within the fi rst few days
following the inciting injury.
Two primary choices in treatment exist once
the diagnosis is made:
1. vitreous aspiration for culture with intravit-
real injection of antibiotics
2. pars plana vitrectomy with intravitreal injec-
tion of antibiotics.
The preferred treatment strategy depends on
multiple variables including the status of the lens
and posterior segment. Chapter 14 discusses in
further detail the controversy surrounding the
management of traumatic endophthalmitis.
The prophylactic use of antibiotics in the peri-
operative period of an open globe injury is some-

what controversial, although nearly universally
utilized. Some studies have shown a decline in
post-traumatic endophthalmitis rates with the
routine use of prophylactic antibiotics.23 However,
the antibiotic selection and preferred route of
delivery vary greatly from practitioner to practi-
tioner. Topical antibiotics are used in all cases
and are often supplemented with intravenous,
subconjunc-tival, intracameral, intravitreal or
oral antibiotics. Chapter 14 discusses the contro-
CASE EXAMPLES
Case report: traumatic endophthalmitis (Figure 13.5)
A 60-year-old male slipped on the lower rungs of a
ladder and in an effort to stabilize himself acciden-
tally stabbed himself in the left eye with a sharpened
pencil he was holding. Initial examination of the left
eye revealed a visual acuity of hand motions and an
intraocular pressure of 7 (compared to 19 in the
fellow eye). Slit lamp examination revealed an infero-
temporal conjunctival laceration overlying a likely
scleral laceration. A small hyphema was present in
the anterior chamber and no view of the posterior
pole was possible due to vitreous hemorrhage (A).
A B
Delayed complications of ocular injury
versy surrounding the prophylactic treatment
of post-traumatic endophthalmitis in further
detail along with authors’ recommendations for
treatment.
The visual prognosis for post-traumatic endo-
phthalmitis is often poor. Multiple studies have
shown a wide range of visual outcomes, mostly
dependent on the virulence of the organisms
isolated. Visual acuity ≥ 20/400 was seen in
22–75% of cases.17,18,21,22,24,25
A CT scan was performed to rule out an intraocular
foreign body. The patient was taken to the operating
room where the scleral laceration was closed
and a pars plana lensectomy and vitrectomy was
performed. The patient presented 5 days after
surgery with increasing pain and nausea. Visual
acuity was bare light perception and intraocular
pressure was 25. Slit lamp examination revealed
severe conjunctival injection, corneal edema, and a
small layered hypopyon (B). A diagnosis of traumatic
endophthalmitis was made. A vitreous aspirate was
205
 Ocular trauma
Case report: traumatic endophthalmitis (cont’d)
obtained for culture and intravitreal antibiotics were
injected (vancomycin and ceftazidime). Cultures
began growing Candida albicans 3 days after the
sample was collected. Despite future intravitreal
injections of amphotericin B and voriconazole along
with oral fluconazole, the patient deteriorated to
bare light perception vision with severe, debilitating
pain (C). After an extensive discussion with the
C D
CONCLUSIONS
It is difficult to give specifics on the appropriate
interval for follow-up after ocular trauma because
of the immense diversity in presentation and
severity. Follow-up must be tailored to the indi-
vidual situation. The authors recommend goni-
oscopy and dilated fundus examination in every
patient with ocular trauma a month after pre-
sentation if the inciting injury was of significant
force to cause intraocular inflammation (iritis)
or disruption (commotio retinae). Of particular
concern are high-velocity contusive injuries.
Gonioscopy is performed to determine if angle
recession has occurred. A dilated fundus exami-
nation is important to evaluate the lens for cata-
ract and the peripheral retina for possible tears,
dialyses, or detachments.
206
patient, the decision was made to enucleate the
injured eye. Gross pathologic examination revealed
extensive fungal involvement in the retina, vitreous,
ciliary body, and anterior chamber (D). The patient
did well following enucleation with complete resolu-
tion of pain. Polycarbonate spectacles were pre-
scribed for full-time use.
SUMMARY
1. Red blood cell breakdown products can cause
glaucoma by directly blocking the trabecular
meshwork.
2. Iron- and copper-containing foreign bodies
can lead to severe toxic reactions in the eye if
not expediently removed.
3. Sympathetic ophthalmia is a feared complica-
tion of ocular trauma and often directs the
management of the severely injured eye.
4. The incidence of traumatic endophthalmitis
has fallen since the widespread use of prophy-
lactic antibiotics in the setting of an open
globe, although the selection and route of
antibiotic delivery remains controversial.
 Delayed complications of ocular injury

REFERENCES 15. Brinton GS, Topping TM, Hyndiuk RA, et al. Posttraumatic
endophthalmitis. Arch Ophthalmol 1984;102:547–550.
16. Verbraeken H, Rysselaere M. Post-traumatic endophthalmitis.
1. Begle HL. Perforating injuries of the eye by small steel
European J Ophthalmol 1994;4:1–5.
fragments. Am J Ophthalmol 1929:12:970–977.
17. Essex RW, Yi Q, Charles PGP, Allen PJ. Post-traumatic
2. Tawara A. Transformation and cytotoxicity of iron in siderosis
endophthalmitis. Ophthalmol 2004;111:2015–2022.
bulbi. Invest Ophthalmol Vis Sci 1986:27:226–236.
18. Thompson WS, Rubsamen PE, Flynn HW Jr., Schiffman J,
3. Talamo JH, Topping TM, Maumenee AE, Green WG.
Cousins SW. Endophthalmitis after penetrating trauma:
Ultrastructural studies of cornea, iris and lens in a case of
risk factors and visual acuity outcomes. Ophthalmol
siderosis bulbi. Ophthalmology 1985;92:1675–1680.
1995;102:1696–1701.
4. Davidson M. Siderosis bulbi. Am J Ophthalmol
19. Soheilian M, Rafati N, Peyman GA. Prophylaxis of acute
1933;16:331–335.
posttraumatic bacterial endophthalmitis with or without
5. Kuhn F, Witherspoon CD, Morris R, Skalka H. Improvement of
combined intraocular antibiotics: a prospective, double-
siderotic ERG. Eur J Ophthalmol 1992;2:44–45.
masked randomized pilot study. Int Ophthalmol 2001;24:
6. Duke-Elder S, MacFaul PA: Injuries: mechanical injuries.
323–330.
In: Duke-Elder S, ed. System of Ophthalmology. St Louis:
20. Kunimoto DY, Das T, Sharma S, et al. Microbiologic spectrum
CV Mosby Co, 1972;14:512–523.
and susceptibility of isolates: part II. Posttraumatic
7. Beckerman BL. Intraocular foreign body extraction in early
endophthalmitis. Am J Ophthalmol 1999;128:242–244.
chalcosis. Arch Ophthalmol 1972;87:444–446.
21. Abu El-Asrar AM, Al-Amro SA, Al-Mosallam AA,
8. Rosenthal AR, Marmor MF, Leuenberger P. Chalcosis: a study
Al-Obeidan S. Post-traumatic endophthalmitis: causative
of natural history. Ophthalmology 1979;86:1956–1972.
organisms and visual outcome. European J Ophthalmol
9. Pollack AL, Mcdonald HR, Ai E, et al. Sympathetic ophthalmia
1999;9:21–31.
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
Ocular trauma remains a prevalent and largely
preventable cause of visual morbidity. As you
have read in previous chapters, traumatic injuries
of the globe range from simple corneal abrasions
to complex corneoscleral lacerations. Such inju-
ries are suffered by children and adults of all
ages, in the home as well as at work and on holi-
days. While the types of eye trauma suffered by
patients and the treatment concerns of clinicians
are similar to those of years past, treatment
options and technology have undergone a tre-
mendous evolution. Due to the unpredictable,
varied and often urgent nature of ocular trauma,
a paucity of prospective outcomes data exists
and controversies persist. Below, we present a
discussion of current topics in ocular trauma,
with particular attention to controversies over
management. Most controversies involve differ-
ences in opinion on the best way to preserve
vision while minimizing the number of surgeries
and avoiding undue stress on a compromised
eye.
The subjects discussed in this section are
advanced issues and are directed primarily at the
sub-specialist ophthalmologist who will be inter-
vening surgically. The timing and extent of initial
surgical intervention has long been controversial
and most eye surgeons who deal with surgical
eye trauma base their methods on experience
and anecdotal information. It will be difficult to
ever have a defi nitive answer to many of these
questions given the lack of similarity from injury
to injury and the resultant difficulty in planning
and carrying out any sort of prospective study.
14
Nevertheless, maintaining an ongoing discourse
on these subjects will hopefully lead to consen-
sus agreements on the most appropriate methods
of medical and surgical intervention, even if true
prospective data are unavailable. It is for these
reasons that this chapter has been included, not
to give defi nitive answers, but to continue the
dialogue.
INTRAOCULAR FOREIGN
BODY REMOVAL
Intraocular foreign body (IOFB) is an uncom-
mon type of ocular trauma but accounts for a
large portion of the cases requiring extensive
surgical intervention. The epidemiology, patho-
physiology, evaluation and initial management of
an IOFB have been thoroughly discussed in
Chapter 12. However, significant controversies
exist concerning the timing of posterior segment
IOFB removal and the most appropriate method
of foreign body removal, especially with mag-
netic intraocular foreign bodies.
Timing of IOFB removal
Several items often dictate the timing of IOFB
removal:
1. IOFB composition and toxicity
2. the risk of infection
3. the presence or absence of a posterior vitreous
detachment (PVD)
4. the risk of suprachoroidal hemorrhage.
The composition of a foreign body determines
the potential for toxicity, inflammation, or infec-
tion, thereby dictating the immediacy of surgical
intervention. If the foreign substance is soil,
209
 Ocular trauma
vegetable matter, or copper, then few would dis-
pute the need for immediate removal given the
tremendous risk of infection with organic mate-
rial and the severe toxic reactions encountered
with copper foreign bodies (see Chapter 13).
With foreign bodies that have less potential for
ocular toxicity (e.g. glass, plastic, or steel), the
issue becomes less clear. Some practitioners
advocate postponing IOFB removal until a PVD
can be documented by examination or ultra-
sound, and the risk of choroidal hemorrhage is
decreased.1–4
Advocates for immediate foreign body removal
cite the risk of intraocular infection as being
too high (3–17%) to wait for a PVD to occur
without an unacceptable risk of permanent vision
loss.5–17 Theoretically, by removing the IOFB
and using antibiotics within 24 hours of the
injury, it is possible to significantly reduce
the risk of infection.5,9,10 In addition, immediate
IOFB removal limits the formation of fibrin
around the IOFB, thereby facilitating removal.
Another argument for early removal is earlier
recovery. Once a patient sustains injury from
an IOFB, the road to recovery can be long and
fi lled with multiple surgeries. If removal of the
IOFB is possible at the time of primary closure,
healing and visual recovery can sometimes be
expedited.18
Vitreoretinal surgeons in favor of delayed IOFB
removal prefer waiting for a spontaneous PVD
which frequently occurs between 10 and 14 days
after the initial injury. Waiting for a PVD is
reasonable, particularly in young patients where
a pre-existing PVD is unlikely and creating a
mechanical PVD is not always possible. Postop-
eratively, an intact posterior hyaloid face increases
the risk for proliferative vitreoretinopathy and
subsequent tractional retinal detachment.
If delayed IOFB removal or observation is
chosen over immediate removal, several items
must be assured:
210
1. Frequent clinical examinations are necessary
to detect evolving retinal tears, retinal detach-
ment, ocular toxicity and infection. If a
view of the posterior pole is limited by
vitreous hemorrhage, traumatic cataract or
corneal opacity, then serial ultrasounds are
necessary.
2. Appropriate coverage with systemic antibiot-
ics with proven intravitreal penetration should
be utilized.
3. If the foreign body is ferrous, serial electro-
retinograms should be performed to detect
signs of toxicity.4
4. Vitrectomy should be performed expedi-
tiously once a PVD has occurred since vitre-
ous organization will occur approximately 14
days post-injury and the risk of tractional
retinal detachments will increase thereafter.
Instrumentation for IOFB removal
The ability to successfully remove foreign bodies
from the posterior segment has advanced over the
years with the progress of surgical technology.
Prior to vitrectomy, an external magnetic was
used for the removal of all magnetic IOFBs.19–21
With external magnets, Snellen visual acuity
of 20/40 was achieved 55–60% of the time.22
However, most authors believe the use of magnets
external to the globe poses unnecessary risks
to the retina, including retinal tears and detach-
ments, vitreous hemorrhage, cataract formation,
new contusion injuries, and retention of
IOFBs.6,18,22,23
With the advent of pars plana vitrectomy, it
became possible to use internal magnets or intra-
ocular forceps to remove foreign bodies from the
posterior segment under direct visualization
(Figure 14.1).8,12 Although a defi nitive study has Included
on DVD
not been performed which demonstrates the
superiority of vitrectomy techniques versus the
use of an external magnet, it is clear that
ancillary damage such as cataracts, vitreous
 Ocular trauma controversies

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
be prevented when using direct visualization
possible only with closed vitrectomy tech-
niques.23 Also, vitrectomy allows for removal of
encapsulated foreign bodies and intraretinal
foreign bodies which may not always be possible
with the use of external magnets.6 Theoretically,
one can also decrease the risk of endophthalmitis
by reduction or removal of the inciting organisms
from the vitreous cavity.5 Despite the more con-
trolled extraction of foreign bodies with vitrec-
tomy, fi nal visual acuity (60% with > 20/40
Snellen visual acuity) when compared to use of
external magnets is similar; however, the rate
of enucleation is lower in the vitrectomy
group.6,22,24,25 In practical terms, the use of exter-
nal magnets has all but stopped in the era of
closed vitrectomy and is primarily of historical
interest.
When a metallic IOFB is present, an intrao-
cular magnet (rare earth magnet) and/or intra-
ocular forceps can be used to lift the IOFB
from the retinal surface once vitreous removal
is complete.8,12 In addition to new surgical
instrumentation, perfluorocarbon can now be
used when non-metallic foreign bodies are
present. This allows ‘floating’ of objects off the
retinal surface. The suspended object can then
be grasped with intraocular forceps and subse-
quently removed without making contact with
the retinal surface.20,21
PROPHYLACTIC SURGICAL TECHNIQUES
IN THE OPEN GLOBE
If an eyewall violation has occurred posterior to
the limbus and vitreous has presented to the
wound, the risk of concurrent or delayed retinal
detachment is high.26–28 Due to this increased
risk of retinal detachment, there is controversy
about repair strategies for posterior globe lacera-
tions or ruptures. Specifically, many surgeons
prefer to primarily close the wound only, while
others place a prophylactic scleral buckle and/or
perform a vitrectomy at the time of primary
wound closure.
Proponents of prophylactic scleral buckling
cite studies showing approximately 60–70% of

211
 Ocular trauma
posteriorly traumatized eyes will eventually
require a scleral buckle.26–28 Vitreous disruption
and/or incarceration at the site of primary injury
leads to vitreous-eyewall adhesions and overlying
vitreous organization and contraction. An adja-
cent or distant tractional retinal detachment
can result from the combined forces of the new
vitreous adhesion to the eyewall, the vitreous
contraction, and the contraction of the posterior
hyaloid (in the absence of a PVD).29,30 By placing
a scleral buckle, it is possible to reduce the ante-
rior–posterior traction that results from vitreous
contraction, theoretically reducing the risk of
tractional retinal detachment. Additionally, an
encircling scleral buckle will reduce the effects
of centripetal forces at the vitreous base that
develop with vitreous contraction and organiza-
tion of the anterior vitreous. Other reports favor
prophylactic scleral buckle placement at the time
of primary repair because ocular muscles are
frequently already exposed during surgical
exploration and future placement can be more
difficult due to subsequent scarring.28
Scleral buckle placement at the time of open
globe repair is not without risks. Since intraocu-
lar pressure may be reduced, the extra manipula-
tion required to place the scleral buckle increases
the chances of a choroidal hemorrhage or extru-
sion of intraocular contents through an occult
posterior eyewall defect. Furthermore, if the
globe anatomy is significantly altered after repair,
anchor scleral suture placement can be more dif-
ficult to execute, and the risk of a full-thickness
suture pass may increase. In addition to the
intraoperative difficulties inherent in placing a
scleral buckle, the usual postoperative issues
such as induced myopia and diplopia remain.
Vitrectomy alone is sometimes advocated at
the time of primary open globe repair. 31–34 Most
agree that vitrectomy benefits eyes with IOFB,
endophthalmitis secondary to trauma, occluded
212
visual axis due a disrupted lens, and in perforat-
ing ocular injuries.5,6,8,18,24,32,33,35–39 In performing
a primary vitrectomy, potential areas of vitreo-
retinal adhesion can be eliminated, theoretically
reducing the likelihood of a delayed tractional
retinal detachment. 30,40–42 However, performing
vitrectomy at the time of primary repair can be
difficult. Challenges in primary vitrectomy
include induction of a PVD mechanically (par-
ticularly in young patients), a limited view of the
posterior segment due to poor corneal clarity,
concern for a large choroidal hemorrhage and the
inability to maintain a constant intraocular pres-
sure if leakage occurs at a penetrating or perfo-
rating injury site. 36
Alternatively, some practitioners advocate
early vitrectomy, but not at the time of primary
globe repair. In this case, a delayed vitrectomy
is performed approximately 7–10 days after
injury.26,27,36 Proponents feel that posterior vitre-
ous separation has likely occurred while signifi-
cant vitreous organization and contraction has
yet to occur. In addition, if subretinal and/or
choroidal hemorrhage is present, then delaying
vitrectomy permits spontaneous resolution.
Finally, delaying vitrectomy allows time for
reduction in uveal congestion, which theoreti-
cally reduces the incidence of intraoperative
hemorrhage. 36
Finally, whether to use a scleral buckle and
pars plana vitrectomy despite the absence of a
retinal detachment is also controversial. Argu-
ments for using a scleral buckle at the time of
vitrectomy include:
1. The retinal periphery is often difficult to visu-
alize and peripheral pathology can possibly be
missed.24,43
2. A scleral buckle gives support to the vitreous
base as the vitreous contracts.24,43
3. A scleral buckle can prevent traction on the
vitreous base created by incarcerated vitreous

in the sclerotomies or at the initial injury
site.24,43,44
Most studies suggest that adding a scleral
buckle at the time of vitrectomy can reduce the
chance of a retinal detachment two to three
times.1,26,27,43,45–47 However, confl icting results
have done little to ameliorate the controversy.48
INTRAOCULAR LENS IMPLANTATION
DURING OPEN GLOBE REPAIR
Traumatic cataracts are a common occurrence
with open globe injuries. If the crystalline lens
is removed at the time of primary repair, then
the decision to place an intraocular lens (IOL)
at the time of the surgery has to be made. Con-
current IOL placement may allow for more
rapid visual rehabilitation. Most published
reports have limited investigation to cases in
which the trauma involves only the anterior
segment or the eyewall violation is confi ned to
the cornea.49–53 When lacerations or ruptures
extend beyond the limbus, the rate of complex
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
selection are required before IOL implantation.
The authors recommend limiting primary IOL
implantation to eyes where the eyewall violation
is limited to the cornea, there is an absence of
Ocular trauma controversies
retinal detachment, and there are no signs of
endophthalmitis.
ENDOPHTHALMITIS
Prophylaxis
In evaluating treatment options for an open
globe injury, the practitioner must determine
whether antibiotics are necessary as a preventa-
tive measure. Endophthalmitis following an open
globe injury occurs in 2–13% of cases (Figure
14.2).14,54 In eyes with retained intraocular
foreign bodies, the rate of endophthalmitis is
usually even higher (7–30%), particularly if
organic contaminants are introduced into the
eye.5–17 Currently, in the setting of an open globe,
antibiotics are often used despite the lack of
defi nitive evidence to support the practice.
Determining the spectrum of coverage and route
of delivery are thus the main questions that
arise.
When choosing an antibiotic, the spectrum of
coverage is most frequently determined accord-
Figure 14.2 This 17-year-old male developed fulminate
endophthalmitis following ruptured globe repair. No
prophylactic intraocular antibiotics were used at the
time of repair. Controversy exists as to whether such
cases could be minimized with the routine use of
prophylactic intraocular antibiotics.
213
 Ocular trauma
ing to the method of injury and the organism
found most frequently in that type of injury. For
example, in trauma, the most common organism
is Staphylococcus epidermis (20.8%). Propionibac-
terium acnes (14.6%), other coagulase negative
Staphylococcus species and Streptococcus viridans
group (12.5%) species are also prevalent, though
infections from the last are found more often in
children than in adults.54 Aerobic gram positive
rods (12.5–25%), such as Bacillus species, are
also cultured with regularity in open globe inju-
ries, more commonly associated with injuries
involving soil contamination.54
Though most practitioners employ subcon-
junctival antibiotics following open globe repair,
there is no consensus about the necessity for
intravitreal antibiotics. In cases where there is a
grossly contaminated wound or a high index of
suspicion for organic contamination, the use of
intravitreal antibiotics is warranted. Vancomycin
and cefazolin have good gram positive coverage.
Ceftazidime has good gram negative coverage.
Aminoglycosides are usually contraindicated
intravitreally due to retinal toxicity. Animal
models suggest that fluroquinolones can be used
and can provide broad-spectrum microbial cov-
erage. Caution is necessary with any intravitreal
injection if the view of the posterior pole is
obscured. Inadvertent injection into the wrong
compartment of the eye can occur due to unrec-
ognized hemorrhagic or serous choroidal detach-
ments. Direct retinal toxicity from the antibiotics
is also a concern, particularly if full doses of
intravitreal antibiotics are used in an eye with a
decreased vitreous volume (e.g. traumatic retinal
detachment).
In the setting of open globe injury, the authors
recommend the use of intraocular antibiotics in
certain high-risk clinical settings, such as intra-
ocular foreign body, a dirty wound involving
plant or vegetable matter, or a wound involving
the lens. Antibiotics are typically injected
214
directly into the vitreous cavity 3–4 millimeters
posterior to the limbus. Our fi rst line choice of
intravitreal antibiotics in a traumatic setting are
vancomycin (1 mg in 0.1 cc) and ceftazidime
(2.25 mg in 0.1 cc). We prefer to inject antibiot-
ics at the end of the case, after the wound is
closed. With the availability of a fourth-
generation fluoroquinolone with known intravit-
real penetration and broad-spectrum coverage,
the authors also recommend both peri- and post-
operative oral antibiotic coverage. Specifically,
we prefer to dose gatifloxacin 400 mg daily by
mouth for 7–10 days after surgery.
Management
Management of post-traumatic (as well as post-
operative) endophthalmitis remains contro-
versial despite a prospective, randomized,
multicenter study. The Endophthalmitis Vitrec-
tomy Study (EVS) investigated the issue in the
non-traumatic post-cataract surgery setting.
In the EVS, vitreous tap and injection appeared
as effective as vitrectomy when the visual
acuity is equal to or better than hand motions
at presentation. Eyes with light perception
vision fared better with vitrectomy.55 Whether
the results of the EVS can be extrapolated
into other clinical scenarios such as trauma is
unknown.
In post-traumatic endophthalmitis, the ratio-
nale for vitrectomy over vitreous tap and injec-
tion is the mechanical removal of toxins, debris,
and infectious organisms. Removing the vitreous
may also allow better dispersion of antibiotics in
the vitreous cavity.
In cases of traumatic endophthalmitis, the
authors typically recommend vitrectomy if a safe
view of the posterior segment is at all possible,
as most patients with traumatic endophthalmitis
will eventually require vitrectomy for visual
rehabilitation.

PRIMARY ENUCLEATION AFTER SEVERE
OCULAR TRAUMA
In cases of severe ocular trauma resulting in
severe loss of ocular tissue, complete destruction
of the globe, expulsive choroidal hemorrhage, or
severing of the optic nerve, the chances of visual
recovery can be zero. In cases where visual recov-
ery is not possible following severe ocular trauma,
previous studies have recommended enucleation
within 2 weeks due to the risk of sympathetic
ophthalmia. Most cases of sympathetic ophthal-
mia occur between 2 weeks and 3 months (65–
80%) post-trauma.56,57
Loss of light perception is not a contrain-
dication to globe-salvaging surgical repair, as
reversal of loss of light perception has been
reported.58 Multiple factors, including anato-
mical status of the injured eye, mental status of
the patient, and status of the other eye should
be considered in determining the appropriate
surgical plan.
Controversy exists over the use of enucleation
as a primary procedure. When patients have sus-
tained severe and irreparable injuries to the
globe, they are often sedated with pain medica-
tions, unconscious, or even intoxicated. Due to
their altered mental status, they may be tempo-
rarily incapable of comprehending the severity of
their injuries, and may also be incapable of giving
informed consent for globe repair, much less
removal. In such cases, most practitioners advo-
cate a primary closure attempt. If the globe
cannot be closed, enucleation can be discussed
after restoration of decision-making ability. At
this time, patients are more likely to understand
the discussion, and will have the opportunity to
determine for themselves that the injured globe
cannot see. If an injured globe is damaged beyond
repair and the patient is alert and capable of
making an informed decision, primary enucle-
ation may be considered. Such a decision must
Ocular trauma controversies
be made on an individual basis with careful con-
sideration to the individual patient and the status
on the injured globe. In our experience this is an
unusual occurrence typically reserved for devas-
tating injuries with massive loss of tissue (e.g.
gunshot wounds).
SUMMARY
1. The timing of IOFB removal is dictated by
IOFB composition, risk of infection, and sur-
gical risks.
2. Vitrectomy has revolutionized the removal
of ferromagnetic posterior segment IOFB,
although an improved rate of visual acuity
outcomes has never been shown compared to
use of an external magnet.
3. IOL implantation at the time of open globe
repair is typically reserved for traumatic cata-
racts associated with lacerations or ruptures
confi ned to the cornea.
4. Although controversial, prophylactic scleral
buckle following open globe injury may
decrease the rate of subsequent retinal detach-
ment, particularly when vitreous incarcera-
tion of the wound is encountered.
5. Theoretic advantages of vitrectomy for post-
traumatic endophthalmitis include mechani-
cal removal of debris and infectious material
as well as better dispersion of intravitreal
antibiotics.
6. Primary enucleation following open globe
injury is seldom performed.
REFERENCES
1. Hutton WL. Pars plana vitrectomy: the role of vitrectomy in
penetrating ocular injuries. Trans Sect Ophthalmol Am Acad
Ophthalmol Otolaryngol 1976;81:414–419.
2. Knave B. The ERG and ophthalmological changes in
experimental metallosis in the rabbit. II. Effects of steel,
copper and aluminium particles. Acta Ophthalmol (Copenh)
1970;48(1):159–173.
215
 Ocular trauma
3. Knave B. The ERG and ophthalmological changes in
experimental metallosis in the rabbit. I. Effects of iron
particles. Acta Ophthalmol (Copenh) 1970;48(1):136–158.
4. Sneed SR, Weingeist TA. Management of siderosis bulbi due
to a retained iron-containing intraocular foreign body.
Ophthalmology 1990;97(3):375–379.
5. Mieler WF, Ellis MK, Williams DF, Han DP. Retained intraocular
foreign bodies and endophthalmitis. Ophthalmology
1990;97(11):1532–1538.
6. Williams DF, Mieler WF, Abrams GW, Lewis H. Results and
prognostic factors in penetrating ocular injuries with
retained intraocular foreign bodies. Ophthalmology
1988;95(7):911–916.
7. Boldt HC, Pulido JS, Blodi CF, Folk JC, Weingeist TA. Rural
endophthalmitis. Ophthalmology 1989;96(12):1722–1726.
8. Coleman DJ, Lucas BC, Rondeau MJ, Chang S. Management
of intraocular foreign bodies. Ophthalmology 1987;94(12):
1647–1653.
9. Thompson JT, Parver LM, Enger CL, Mieler WF, Liggett PE.
Infectious endophthalmitis after penetrating injuries with
retained intraocular foreign bodies. National Eye Trauma
System. Ophthalmology 1993;100(10):1468–1474.
10. Jonas JB, Knorr HL, Budde WM. Prognostic factors in ocular
injuries caused by intraocular or retrobulbar foreign bodies.
Ophthalmology 2000;107(5):823–828.
11. Affeldt JC, Flynn HW, Jr., Forster RK, Mandelbaum S, Clarkson
JG, Jarus GD. Microbial endophthalmitis resulting from ocular
trauma. Ophthalmology 1987;94(4):407–413.
12. De Souza S, Howcroft MJ. Management of posterior segment
intraocular foreign bodies: 14 years’ experience. Can J
Ophthalmol 1999;34(1):23–29.
13. Behrens-Baumann W, Praetorius G. Intraocular foreign bodies:
297 consecutive cases. Ophthalmologica 1989;198(2):84–88.
14. Brinton GS, Topping TM, Hyndiuk RA, Aaberg TM, Reeser FH,
Abrams GW. Posttraumatic endophthalmitis. Arch
Ophthalmol 1984;102(4):547–550.
15. Khan MD, Kundi N, Mohammed Z, Nazeer AF. A 6 1/2-years
survey of intraocular and intraorbital foreign bodies in the
North-west Frontier Province, Pakistan. Br J Ophthalmol
1987;71(9):716–719.
16. Armstrong MF. A review of intraocular foreign body injuries
and complications in N. Ireland from 1978–1986. Int
Ophthalmol 1988;12(2):113–117.
17. Punnonen E, Laatikainen L. Prognosis of perforating eye
injuries with intraocular foreign bodies. Acta Ophthalmol
(Copenh) 1989;67(5):483–491.
18. Friberg TR. Long-term visual acuity results after penetrating
and perforating ocular injuries. Am J Ophthalmol 1986;101(4):
499–500.
216
19. Percival SP. A decade of intraocular foreign bodies. Br J
Ophthalmol 1972;56(6):454–461.
20. Roper-Hall MJ. Review of 555 cases of intra-ocular foreign
body with special reference to prognosis. Br J Ophthalmol
1954;38(2):65–99.
21. Johnston S. Perforating eye injuries: a five year survey.
Trans Ophthalmol Soc UK 1971;91:895–921.
22. Shock JP, Adams D. Long-term visual acuity results after
penetrating and perforating ocular injuries. Am J Ophthalmol
1985;100(5):714–718.
23. Amalong RJ. Retinal detachment after manipulation of
magnetic foreign body. Am J Ophthalmol 1970;70(1):
10–13.
24. Spalding SC, Sternberg P, Jr. Controversies in the
management of posterior segment ocular trauma.
Retina 1990;10(Suppl. 1):S76–82.
25. de Juan E, Jr., Sternberg P, Jr., Michels RG, Auer C. Evaluation
of vitrectomy in penetrating ocular trauma: a case-control
study. Arch Ophthalmol 1984;102(8):1160–1163.
26. Hutton WL, Fuller DG. Factors influencing final visual
results in severely injured eyes. Am J Ophthalmol
1984;97(6):715–722.
27. Brinton GS, Aaberg TM, Reeser FH, Topping TM, Abrams GW.
Surgical results in ocular trauma involving the posterior
segment. Am J Ophthalmol 1982;93(3):271–278.
28. Stone TW, Siddiqui N, Arroyo JG, McCuen BW, 2nd, Postel EA.
Primary scleral buckling in open-globe injury involving the
posterior segment. Ophthalmology 2000;107(10):1923–1926.
29. Hsu HT, Ryan SJ. Natural history of penetrating ocular injury
with retinal laceration in the monkey. Graefes Arch Clin Exp
Ophthalmol 1986;224(1):1–6.
30. Cleary PE, Ryan SJ. Method of production and natural history
of experimental posterior penetrating eye injury in the rhesus
monkey. Am J Ophthalmol 1979;88(2):212–220.
31. Coleman DJ. Early vitrectomy in the management
of the severely traumatized eye. Am J Ophthalmol
1982;93(5):543–551.
32. Coles WH, Haik GM. Vitrectomy in intraocular trauma: its
rationale and its indications and limitations. Arch Ophthalmol
1972;87(6):621–628.
33. Faulborn J, Atkinson A, Olivier D. Primary vitrectomy as a
preventive surgical procedure in the treatment of severely
injured eyes. Br J Ophthalmol 1977;61(3):202–208.
34. de Juan E, Jr., Sternberg P, Jr., Michels RG. Timing of
vitrectomy after penetrating ocular injuries. Ophthalmology
1984;91(9):1072–1074.
35. Conway BP, Michels RG. Vitrectomy techniques in the
management of selected penetrating ocular injuries.
Ophthalmology 1978;85(6):560–583.

36. Ryan SJ, Allen AW. Pars plana vitrectomy in ocular trauma.
Am J Ophthalmol 1979;88:483–491.
37. Coleman DJ. Pars plana vitrectomy: the role of vitrectomy in
traumatic vitreopathy. Trans Sect Ophthalmol Am Acad
Ophthalmol Otolaryngol 1976;81:406–413.
38. Benson WE, Machemer R. Severe perforating injuries treated
with pars plana vitrectomy. Am J Ophthalmol 1976;81(6):
728–732.
39. Mieler WF, Mittra RA. The role and timing of pars plana
vitrectomy in penetrating ocular trauma. Arch Ophthalmol
1997;115(9):1191–1192.
40. Cleary PE, Ryan SJ. Vitrectomy in penetrating eye injury:
results of a controlled trial of vitrectomy in an experimental
posterior penetrating eye injury in the rhesus monkey. Arch
Ophthalmol 1981;99(2):287–292.
41. Topping TM, Abrams GW, Machemer R. Experimental double-
perforating injury of the posterior segment in rabbit eyes: the
natural history of intraocular proliferation. Arch Ophthalmol
1979;97(4):735–742.
42. Abrams GW, Topping TM, Machemer R. Vitrectomy for injury:
the effect on intraocular proliferation following perforation of
the posterior segment of the rabbit eye. Arch Ophthalmol
1979;97(4):743–748.
43. Ahmadieh H, Soheilian M, Sajjadi H, Azarmina M, Abrishami
M. Vitrectomy in ocular trauma: factors influencing final visual
outcome. Retina 1993;13(2):107–113.
44. Michels RG. Vitrectomy methods in penetrating ocular
trauma. Ophthalmology 1980;87(7):629–645.
45. Miyake Y, Ando F. Surgical results of vitrectomy in ocular
trauma. Retina 1983;3(4):265–268.
46. Haut J, Allagui M, Lepvrier N, Morel C. Preventive surgical
scleral buckling of retinal detachment after severe ocular
injuries. J Fr Ophtalmol 1993;16(12):668–672.
47. Rosner M, Bartov E, Treister G, Belkin M. Prophylactic scleral
buckling in perforating ocular injuries involving the posterior
segment. Ann Ophthalmol 1988;20(4):146–149.
48. Hermsen V. Vitrectomy in severe ocular trauma.
Ophthalmologica 1984;189(1–2):86–92.
Ocular trauma controversies
49. Rubsamen PE, Irvin WD, McCuen BW, 2nd, Smiddy WE,
Bowman CB. Primary intraocular lens implantation in the
setting of penetrating ocular trauma. Ophthalmology
1995;102(1):101–107.
50. Bowman RJ, Yorston D, Wood M, Gilbert C, Foster A. Primary
intraocular lens implantation for penetrating lens trauma in
Africa. Ophthalmology 1998;105(9):1770–1774.
51. Lamkin JC, Azar DT, Mead MD, Volpe NJ. Simultaneous
corneal laceration repair, cataract removal, and posterior
chamber intraocular lens implantation. Am J Ophthalmol
1992;113(6):626–631.
52. Chan TK, Mackintosh G, Yeoh R, Lim AS. Primary posterior
chamber IOL implantation in penetrating ocular trauma.
Int Ophthalmol 1993;17(3):137–141.
53. Anwar M, Bleik JH, von Noorden GK, el-Maghraby AA, Attia F.
Posterior chamber lens implantation for primary repair of
corneal lacerations and traumatic cataracts in children.
J Pediatr Ophthalmol Strabismus 1994;31(3):157–161.
54. Benz MS, Scott IU, Flynn HW, Jr., Unonius N, Miller D.
Endophthalmitis isolates and antibiotic sensitivities:
a 6-year review of culture-proven cases. Am J Ophthalmol
2004;137(1):38–42.
55. Results of the Endophthalmitis Vitrectomy Study. A
randomized trial of immediate vitrectomy and of intravenous
antibiotics for the treatment of postoperative bacterial
endophthalmitis. Endophthalmitis Vitrectomy Study Group.
Arch Ophthalmol 1995;113(12):1479–1496.
56. Gass JD. Sympathetic ophthalmia following vitrectomy. Am J
Ophthalmol 1982;93(5):552–558.
57. Albert DM, Diaz-Rohena R. A historical review of sympathetic
ophthalmia and its epidemiology. Surv Ophthalmol 1989;34(1):
1–14.
58. Kangas TA, Bennett SR, Flynn HW, Jr., et al. Reversible loss of
light perception after vitreoretinal surgery. Am J Ophthalmol
1995;120(6):751–756.
217