PutrtvaflfbpiaisTsa“npim

d

s

B

©

0

d

J Oral Maxillofac Surg66:1913-1920, 2008

Acute Proptosis in Trauma: RetrobulbarHemorrhage or Orbital Compartment

Syndrome—Does It Really Matter?Michael Perry, FRCS, FDS, BSc*

Purpose: To review the nature and outcomes of acute severe proptosis in patients after craniofacialtrauma, over a 6-year period.

Patients and Methods: These were identified prospectively. The mechanism of injury, nature of theproptosis, and visual outcomes in each case were reviewed. Review of the literature was undertaken.

Results: In all cases proptosis, was secondary to retrobulbar edema and not hemorrhage.

Conclusions: Many cases of “retrobulbar hemorrhage” may, in fact, be secondary to edema. This hassignificant implications when managing the proptosed eye on an emergent basis. Possible reasons forpoor outcomes are discussed. A number of unanswered questions arise from this review.© 2008 American Association of Oral and Maxillofacial Surgeons

J Oral Maxillofac Surg 66:1913-1920, 2008

hu

dmaostbgpgdop

sstnreaRtdastmf

roptosis after trauma has been reported to occur inp to 3% of craniofacial injuries.1 However, vision-hreatening proptosis is generally considered to be aare event. Nevertheless, when it occurs, urgent in-ervention is required if loss of vision is to be pre-ented. The orbit is a (mostly) rigid box, exceptnteriorly where the orbital septum and eyelids areexible. Despite its fissures and foramina it seems toollow similar pressure-volume relationships as otherody compartments,2 and is therefore at risk of com-artment syndrome phenomena.3 If bleeding or swell-

ng occurs behind the globe, there is little capacity toccommodate this additional volume, resulting in anncrease in interstitial pressure, fall in perfusion pres-ure, and a degree of anterior globe displacement.he return of vision reported after decompression,uggests ischemia and re-establishment of perfusionre key factors in pathogenesis and management.4,5

Critically” raised retrobulbar pressures thereforeeed to be clearly defined, recognized, and treatedromptly. With “critically” raised pressures, irrevers-

ble optic and retinal ischemia can occur within 60inutes,6,7 and permanent visual loss within 1.5-2

*Consultant Oral and Maxillofacial Surgeon, Ulster Hospital, Dun-

onald, Belfast, United Kingdom.

Address correspondence and reprint requests to Dr Perry: Con-

ultant Oral and Maxillofacial Surgeon, Ulster Hospital, Dundonald,

elfast BT16 1RH, UK; e-mail: mikepmaxfax@yahoo.com

2008 American Association of Oral and Maxillofacial Surgeons

278-2391/08/6609-0019$34.00/0

soi:10.1016/j.joms.2008.04.012

1913

ours.8-10 It is generally accepted that outcomes aresually better the earlier treatment is started.Proptosis after trauma has a number of well-

escribed causes, each of which requires differentanagement if effective decompression is to be

chieved. These include bony displacement into therbit (blow-in fracture),10-12 bleeding into the orbit,13

welling of the retrobulbar contents,14 and extravasa-ion of radiographic contrast material.15 It has alsoeen described complicating prolonged spinal sur-ery in the prone position.16 Usually proptosis is ap-arent by the time the patient arrives in the emer-ency department, although its development can beelayed.17 Orbital emphysema,18 and caroticocavern-us fistulae have been reported as causes of delayedroptosis after facial injury.19,20

Although all these causes result in loss of visionecondary to ischemia, the treatment required to re-tore perfusion varies. Notably, the differentiation be-ween retrobulbar hemorrhage (RBH) (which mayeed evacuation) and retrobulbar edema (which mayesolve medically, or require a different surgical strat-gy) is important. A common teaching is that thecutely proptosed globe after facial trauma is due toBH, and that this requires prompt recognition and

reatment. Furthermore, treatment should never beelayed to undertake investigations.21 After immedi-te lateral canthotomy and cantholysis, medical mea-ures are instituted while preparing the patient forheater. The main purpose of this study was to deter-ine the true causes of acute proptosis after cranio-

acial trauma, and where possible, determine progno-

is in terms of final visual outcome.

P

tw“nttBpsncahdassdatbu3Swodr

R

Diip

mh“a

csCjuc

Ie

D

w(bsossftdhtpbniehsm

Ar

M

1914 ACUTE PROPTOSIS IN TRAUMA

atients and Methods

This was a prospective study. Patients referred tohe maxillofacial unit after blunt craniofacial traumaere included. Those patients with “severe” or

tense” proptosis were identified for study. The diag-osis of “tense proptosis” was made in the resuscita-ion room, after clinical examination, that is, palpa-ion of the globe, comparing it to the noninjured side.oth the degree of hardness and the amount of actualroptosis were subjectively assessed. Objective as-essment (ie, tonometry and exophthalmometry) wasot possible due either to patients’ overall clinicalonditions (ongoing resuscitation), facial swelling,nd in some cases, lack of equipment. Degree ofardness and pupillary reaction were the main clinicaleterminants of ophthalmic urgency, as these weressumed to represent retrobulbar pressures, perfu-ion, and disturbance in function. The pathology re-ulting in proptosis (RBH, edema, air, and so on) wasetermined after imaging (CT). The orbit was evalu-ted in the axial and coronal planes, specifically forhe presence of blood clot, edema, brain, air, andone. The pathology was verified using Hounsfieldnits. Where possible, visual recovery (at minimum ofmonths) was assessed (light, movement perception,

nellens chart). From the case notes the after dataere obtained: 1) mechanism of injury, 2) presencef multiple injuries, 3) ocular signs in emergencyepartment, 4) CT findings, 5) where possible, visualecovery.

esults

Table 1 summarizes data for points 1, 2, 4, and 5.ue to the severity of the injuries all patients were

ntubated and ventilated either at the scene of thenjury, or shortly after arrival in the emergency de-artment. Therefore, no record of visual acuity was

Table 1. PROSPECTIVE DATA COLLECTED FOR PATIENTS

Patient Mechanism of Injury Associated In

1 Fall from a horse C spine, Long bon2 Fall 20 ft None3 MVC (passenger) Multiple rib, limb4 Kicks to head/face None5 Pedestrian hit by car Chest, abdomen,6 MVC (passenger) Pelvis, C spine7 Pedestrian hit by car Bilateral open low8 Kicked by horse None9 MVC (passenger) Chest, long bone

10 MVC (ejected) Chest, abdomen,

bbreviations: MVC, motor vehicle collision; Partial, partiaemained registered blind.

ichael Perry. Acute Proptosis in Trauma. J Oral Maxillofac Surg 2008

ade. In all cases an initial diagnosis of “retrobulbaremorrhage” was made, on basis of 1) an obvious andtense” proptosed globe, 2) non, or “sluggishly” re-cting pupil.

Chemosis and periorbital bruising was noted in allases, to varying degrees. All patients had obviousigns of coexisting head injuries, and therefore urgentTs were carried out to evaluate for intracranial in-

ury. As part of this imaging, CTs of orbits was alsondertaken. In all patients lateral canthotomy andantholysis was performed at the earliest opportunity.The CT images for all patients are shown in Figure 1.

n all cases, the proptosis was seen to be secondary todema (ICD-9 376.33 or ICD-10 H05.2) and not blood.

iscussion

Traditionally the tense, proptosed, nonseeing eyeith a nonreacting dilated pupil, after facial trauma

or its repair) is considered to be because of acuteleeding within the orbit-retrobulbar hemorrhage. Asuch, this is a surgical emergency which, dependingn the patient’s general condition and likelihood ofalvaging vision, may require immediate decompres-ion. Unfortunately, being such a rare condition, veryew of us (including this author) are true experts inhis area, making clear evidenced-based guidelinesifficult to establish. However, the patients describedere clearly show that not all cases of “tense” prop-osis after trauma are because of RBH. Instead, theseroptoses were secondary to edema of the retrobul-ar tissues, resulting in a compartment syndrome phe-omenon. The poor outcomes seen here are in keep-

ng with the reported time constraints in re-stablishing perfusion. Vision-threatening swellingas previously been termed “orbital compartmentyndrome” (OCS),22 which is a very useful term. It isore accurate, and conveys the sense of urgency

CT Findings of Proptosis Visual Recovery

Edema PartialEdema PartialEdema NoneEdema None

lvic Edema DiedEdema None

b Edema NoneEdema PartialEdema None

one Edema None

very. Light or movement perception only; None, patient

juries

e

and pe

er lim

long b

l reco

.

FS

M

MICHAEL PERRY 1915

IGURE 1. A-J, Ten cases of acute, “tense,” proptosis following craniofacial trauma, clinically diagnosed as retrobulbar hemorrhage.ubsequent CT Imaging shows the absence of blood. In all cases, proptosis was due to edema. (Figure 1 continued on next page.)

ichael Perry. Acute Proptosis in Trauma. J Oral Maxillofac Surg 2008.

wt

gm2d(

tv

niciaurs

itietptmrm

nmmirssr

M g 2008

1916 ACUTE PROPTOSIS IN TRAUMA

hen communicating with colleagues unfamiliar inhe management of facial trauma.

Differentiation between RBH and OCS on clinicalrounds alone is not always possible. In both, theain clinical features are 1) decreasing visual acuity,) pain, 3) opthalmoplegia, 4)“tense” proptosis, 5)evelopment of a relative afferent pupillary defectRAPD), 6) swollen or pale optic disc.

In the unconscious or poorly responsive patienthis is limited further to 1) “tense” proptosis, 2) de-elopment of an RAPD, 3) swollen or pale optic disc.Early diagnosis is essential, and often initial exami-

ation is only possible in the emergency department,ntensive care unit, or operating theater. Under theseircumstances assessment is limited and less thandeal. This is even more so if the patient is confused,gitated, or unresponsive. In awake patients, clinicalrgency of proptosis may be determined by deterio-ation in the visual acuity. However, in the uncon-

FIGURE

ichael Perry. Acute Proptosis in Trauma. J Oral Maxillofac Sur

cious or agitated patient this and 2 other useful s

ndicators (pain and ophthalmoplegia) cannot be de-ermined. In unconscious patients, initial assessments therefore restricted to a relatively crude externalxamination, assessment of the pupils, careful palpa-ion of the globes, and if possible, fundoscopy (orortable slit lamp examination). Each has its limita-ions. Often a “tense” proptosed globe with an abnor-ally reacting pupil and swollen disc may be the only

eadily identifiable signs of RBH or orbital compart-ent syndrome.In the vast majority of cases, proptosis is mild and

o active intervention is required. Although exopthal-ometry can be used to measure proptosis, what isore important is whether the optic nerve and retina

s still being adequately perfused. Unfortunately, theelationship between proptosis and retrobulbar pres-ures is not straightforward, especially when one con-iders, by analogy, vision-threatening ischemia in thy-oid eye disease, which can occur in the absence of

nt’d).

.

1 (co

ignificant proptosis. This seemed to be the case in

tgfspdw“ppsaacmaaapetlriqigaeetld

tiiyhmmhbputltpoustdfig

ttpbrhtctsrpdrgsmnstpcpc

bmutbbisFvTpnauTtoVvqsa

pu“di

MICHAEL PERRY 1917

his study—not all of the “tense” proptosed eyes wererossly exophthalmic on the CT images, although in aew cases tension from the optic nerve created theo-called “balloon on a string” sign. One of the mainroblems in the unresponsive patient is thereforeeciding whether a proptosis is “tense” enough toarrant risks of urgent surgery. Proptosis needs to be

quantified” and initially the globes are simply pal-ated. This may not be possible if penetrating orerforating injuries are suspected. Palpation is a veryubjective measure of intraocular pressure, proptosis,nd, by inference, retrobulbar pressures. Terms suchs “stoney hard,” are open to misinterpretation andan mislead. Examination of the pupils can also beisleading in the presence of traumatic mydriasis,

lcohol, illicit drugs, opiates (for pain relief), or par-lyzing agents.23 “Sluggish” pupillary responses arelso very subjective in nature, and open to misinter-retation. Nevertheless, the presence of a correctlylicited RAPD indicates impaired optic nerve func-ion. Only a brisk reaction to direct and consensualight stimuli, in a round, concentric pupil can beegarded as reliable in excluding vision-threateningnjuries requiring immediate intervention. Care is re-uired in the elderly. In some patients, a dilated pupil

tself may precipitate ocular problems.24,25 Acute an-le closure glaucoma can be precipitated by dim light,nd some drugs.26-29 This should be considered in anylderly patient who develops a painful, tense, “redye.” Ideally, fundoscopy should be carried out, al-hough initially this may be unremarkable and mis-eading. Optic atrophy may not be visible for up to 17ays after injury.30

In the cases described, CT scanning was under-aken primarily to assess the patients’ coexisting headnjuries. The role of CT in the assessment of headnjuries has expanded considerably over the last 20ears.31 In the United Kingdom, recent guidelines32

ave encouraged the greater use of CT in the assess-ent of the head-injured patient, and it is now com-only used. With helical scanners, scanning timesave now been reduced significantly.33,34 On thisasis any patient requiring a brain CT, who has sus-ected periorbital or ocular injuries, should ideallyndergo imaging of (at least) the orbits at the sameime. Additional scanning times for this are now neg-igible. Globe rupture, optic nerve transection, in-raocular hemorrhage, intraocular foreign bodies,eriorbital and orbital apex fractures, and the naturef any proptosis are all readily identifiable. B-scanltrasonography is another valuable tool, but does noteem to be used commonly. It is a painless, well-olerated, relatively quick, noninvasive test that canefine orbital masses by their location, size, and con-guration. This may help in the planning of any ur-

ent decompression. a

Orbital CTs only define anatomy, not function, andhey give no measure of tissue perfusion. Portableonometry, used mainly to measure the intraocularressure (IOP), may give some indication of retrobul-ar pressures, although IOP does not precisely reflectetrobulbar pressure.35 Hand-held IOP measurementsave been reported to compare well with Goldmannonometry (gold standard).36 Although the authorould find no reports of the use of tonometry in facialrauma, it would seem to be a more objective (andafer) method than globe palpation. Currently, accu-ate determination of retrobulbar pressure is onlyossible using a “slit catheter” technique enablingirect orbital tissue pressure monitoring, but this is aesearch tool.35,37 Although raised IOP, secondary tolaucoma, can also confuse the issue, it has beenuggested that in a proptosed eye, a pressure of 40mHg or more may indicate critical ischemia and theeed for urgent treatment. By analogy, orthopedicurgeons use an interstitial pressure of 30 mmHg ashe indication of relaxing fasciotomies in acute com-artment syndrome, and pressures of 15 mmHg forhronic compartment syndrome.38 Irrespective of theressures, signs of deteriorating vision (RAPD) indi-ate the need for immediate treatment.The single most important prognostic factor has

een reported to be the amount of damage to theacula or optic nerve at the time of injury.39 Clinical

rgency is therefore usually determined by the pa-ient’s vision.40 In the unconscious patient this cannote determined. Visual-evoked potentials (VEPs) haveeen reliably used to assess the visual pathway.41 VEP

s now well established in the diagnosis of multipleclerosis (MS) and epilepsy, but has limitations.42

lash VEP is regarded as the most reliable predictor ofision, followed by the bright-flash electroretinogram.he value of VEP lies in its ability to identify earlyroblems in the anterior visual pathway, although it isonspecific. It is an objective and reproducible test,nd in craniofacial trauma VEP has been reported as aseful adjunct in early detection of visual loss.43,44

his complements imaging by determining the func-ional impact of any abnormalities adjacent to theptic nerve.41 Up to 90% of patients with positiveEPs have been reported to make complete or partialisual recovery.45 Unfortunately, the equipment re-uired is somewhat cumbersome and not ideallyuited for rapid evaluation in the emergency room,lthough this is not impossible.

CT, tonometry, and flash VEPs therefore have com-lementary roles in the assessment of proptosis in thenconscious patient. Together they help determinewho” needs surgery and “how” it is best done. CTefines anatomy, possible causes of vision-threatening

njuries, and helps plan surgery. Tonometry may give

n indication of urgency by reflecting tissue perfusion

aejtmwptomgts

Wa

daudctt

“MsmrrAavc(

sOpcsrtnttpctimsnb

tilo

m

ochmemfqmtvipTsap

1918 ACUTE PROPTOSIS IN TRAUMA

nd VEP tells us whether vision is at risk and urgentvaluation is required. Nevertheless, sound clinicaludgement is still required to determine which pa-ients may benefit from urgent or emergent treat-ent. Clinical judgement is also required to decidehether it is in the patient’s best interests to post-one treatment until further examination, and inves-igations have precisely determined the extent of thecular/orbital injuries. On the other hand, the treat-ent of some findings (eg, a “very” tense proptosed

lobe) should not be delayed while waiting for inves-igations, and it is in these cases it is argued treatmenthould be commenced as soon as possible.

hy Is the Distinction Between RBHnd OCS Important?

The traditional teaching is that RBH is a clinicaliagnosis necessitating immediate lateral canthotomynd cantholysis, medical measures, and urgent evac-ation of the hematoma. Investigations should notelay treatment.46 Imaging is undoubtedly benefi-ial,47 but as many of us know, may be very difficulto get within the very tight time constraints requiredo save vision.

Medical treatments and a lateral canthotomy46 maybuy time” while preparing the patient for theater.annitol and Acetazolamide48 are frequently pre-

cribed, but in the presence of hypovolaemic shockay be contraindicated. High-dose steroids are also

ecommended but may be contraindicated in view ofecent findings related to their use in head injuries.49

lthough “lateral canthotomy” and “cantholysis” islso recommended, the anatomy and technique isariably described in the literature46,50-52 and may beonfusing to those inexperienced in the techniqueie, most of us).

In those circumstances when urgent decompres-ion is necessary, the distinction between RBH andCS becomes important. If CT scans have not beenerformed, “risk/benefit analysis” is required to de-ide whether decompression is appropriate, safe, andhould be attempted on clinical grounds alone. Inetrobulbar hemorrhage bleeding can be intra- or ex-raconal, the former believed to have a worse prog-osis. Extraconal blood can collect anywhere withinhe extraconal space and may be difficult to accesshrough an inappropriately sited incision. Surgical ap-roaches usually involve a lateral approach as this isonsidered to be safer.46 However, if proptosis is dueo a blood clot medially or it is secondary to edema,nitial exploration will fail to evacuate any clot and

ay result in diagnostic confusion. In such circum-tances an alternative or additional approach mayeed to be considered,53 as decompression must still

e achieved. Patients should not leave the operating r

able until the proptosis has shown obvious signs ofmprovement, or the clinician feels that the sight is noonger salvageable, or other overriding general factorsccur.In those patients where investigations are not im-ediately available a number of questions are raised.

1. When is a proptosis severe enough to warranturgent decompression on clinical groundsalone? Repeated examination is necessary asswelling progresses in the early stages of traumaand vision-threatening proptosis can (in princi-ple and anecdotally) be delayed.

2. When is swelling maximal, and therefore theglobe most at risk? This is not clear in the liter-ature, although 36 hours is sometimes quoted.Furthermore coughing, vomiting, intubation, IVfluids and vasoactive drugs can also precipitatefurther intraocular bleeding and possibly retro-bulbar bleeding.

3. How is decompression best achieved, if the un-derlying cause (bone, blood, edema, air, or fron-tal lobe) is not known?

4. If decompression is not undertaken, can anyresulting chronic ischemia result in muscle fi-brosis and contractures, much akin to the Volk-mann’s ischemic phenomenon?—“Orbital Volk-mann’s.”

5. Does the patient’s systemic blood pressure af-fect orbital perfusion and the decision to decom-press (or not)? In a limb, relative ischemia canoccur at tissue pressures under diastolic bloodpressure.3 In the orbital, for retinal ischemia tooccur, it has been reported that the intraorbitalpressure must exceed the mean arterial pres-sure.22

Irreversible ischemia in OCS is in many ways anal-gous to that seen in the head-injured patient, with aritically raised intracranial pressure. In the severelyead-injured patient it is known that maintaining theean systolic blood pressure above 100 mmHg54,55 is

ssential to improving outcomes. This is necessary toaintain adequate cerebral perfusion pressure. Any

all below this doubles the mortality. This raises theuestion—in the presence of a proptosis, does a lowean systolic blood pressure (after hypovolaemia in

he multiply injured patient) have the same affect onisual disability as it does with neurological disabilityn head injuries? Is there a minimal “orbital perfusionressure” necessary to prevent visual deterioration?his has not been reported in the literature, but hasignificant implications on how (or whether) to treatny proptosis. Sudden and profound episodes of hy-otension from a variety of causes have also been

eported to result in loss of sight56-63 all in the ab-

sa

R

1

1

1

1

1

1

1

1

1

1

2

2

2

2

2

2

2

2

2

2

3

3

3

3

3

3

3

3

3

3

4

4

4

4

4

4

4

4

4

4

MICHAEL PERRY 1919

ence of craniofacial trauma—are these risks greaterfter trauma?

eferences1. Kulkarni AR, Aggarwal SP, Kulkarni RR, et al: Ocular manifes-

tations of head injury: A clinical study. Eye 19:1257, 20052. Peak DA: Acute orbital compartment syndrome 2005. Available

at: http://www.emedicine.com/emerg/topic881.htm. AccessedDecember 2007

3. Patel RV, Haddad FS: Compartment syndromes. Br J Hosp Med66:583, 2005

4. Krausen AS, Ogura JH, Burde RM, et al: Emergency orbitaldecompression: A reprieve from blindness. Otolaryngol HeadNeck Surg 89:252, 1981

5. McCartney DL, Char DH: Return of vision following orbitaldecompression after 36 hours of postoperative blindness. Am JOphthalmol 100:602, 1985

6. Amagasaki K, Tsuji R, Nagaseki Y: Visual recovery followingimmediate decompression of traumatic retrobulbar haemor-rhage via transcranial approach. Neurol Med Chir (Tokyo)38:221, 1998

7. Bailey WK, Kuo PC, Evans LS: Diagnosis and treatment ofretrobulbar haemorrhage. J Oral Maxillofac Surg 51:780, 1993

8. Hayreh SS, Kolder HE, Weingeist TA: Central retinal occlusionand retinal tolerance time. Ophthalmology 87:75, 1980

9. Hislop WS, Dutton GN, Douglas PS: Treatment of retrobulbarhaemorrhage in accident and emergency departments. Br JOral Maxillofac Surg 34:289, 1996

0. Larsen M, Wieslander S: Acute orbital compartment syndromeafter lateral blow-out fracture effectively relieved by lateralcantholysis. Acta Ophthalmol Scand 77:232, 1999

1. Gabrielli MA, Vieira EH, Gabrielli MF, et al: Orbital roof blow-infracture: Report of a case. J Oral Maxillofac Surg 55:1475, 1997

2. Karesh JW, Kelman SE, Chirico PA, et al: Orbital roof “blow-in”fractures. Ophthal Plastic Reconstruct Surg 7:77, 1991

3. Burkat CN, Lemke BN: Retrobulbar hemorrhage: Inferolateralanterior orbitotomy for emergent management. Arch Ophthal-mol 123:1260, 2005

4. Gerbino G, Ramieri A, Nasi A: Diagnosis and management ofretrobulbar haematomas following blunt orbital trauma: A de-scription of eight cases. Int J Oral Maxillofac Surg 34:127, 2005

5. Gerber SL, Duprat G: Orbital compression syndrome after or-bital extravasation of X-ray contrast material. Am J Ophthalmol130:530, 2000

6. Leibovitch I, Casson R, Laforest C, et al: Ischemic orbital com-partment syndrome as a complication of spinal surgery in theprone position. Ophthalmology 113:105, 2006

7. Nissman SA, Pasternak JF: Delayed-onset expulsive choroidalhemorrhage attributed to an acute elevation in systemic bloodpressure following traumatic globe rupture. Ophthal Surg La-sers Imaging 36:340, 2005

8. Jordan D, White C, Anderson R, et al: Orbital emphysema: Apotentially blinding complication following orbital fractures.Ann Emerg Med 17:853, 1988

9. Stanton DC, Kempers KG, Hendler BH, et al: Posttraumaticcarotid-cavernous sinus fistula. J Cranio-Maxillofac Trauma5:39, 1999

0. Stewart MG, Patrinely JR, Appling WD, et al: Late proptosisfollowing orbital floor fracture repair. Arch Otolaryngol HeadNeck Surg 121:649, 1995

1. Li KK, Meara JG, Joseph MP: Reversal of blindness after facialfracture repair by prompt optic nerve decompression. J OralMaxillofac Surg 55:648, 1997

2. Linberg J: Orbital compartment syndromes following trauma.Adv Ophthal Plastic Reconstruct Surg 6:51, 1987

3. Meyer S, Gibb T, Jurkovich GJ: Evaluation and significance ofthe pupillary light reflex in trauma patients. Ann Emerg Med22:1052, 1993

4. Campbell DG: Angle closure glaucoma, an update. PerspectOphthalmol 4:123, 1980

5. Wolfs RC, Grobbee DE, Hofman A, et al: Risk of acute angle-closure glaucoma after diagnostic mydriasis in nonselected

5

subjects: The Rotterdam Study. Invest Ophthalmol Vis Sci38:2685, 1997

6. Ates H, Kayikcioglu O, Andac K: Bilateral angle closure glaucomafollowing general anesthesia. Int Ophthalmol 23:129, 1999

7. Browning AC, Reck AC, Chisholm IH, et al: Acute angle closureglaucoma presenting in a young patient after administration ofparoxetine. Eye 14:406, 2000

8. Hall SK: Acute angle-closure glaucoma as a complication ofcombined beta-agonist and ipratropium bromide therapy in theemergency department. Ann Emerg Med 23:8847, 1994

9. Zenzen CT, Eliott D, Balok EM, et al: Acute angle-closureglaucoma associated with intranasal phenylephrine to treatepistaxis. Arch Ophthalmol 122:655, 2004

0. Gordon S, McCare H: Monocular blindness as a complication ofthe treatment of a malar fracture. Plast Reconstr Surg 6:228, 1950

1. Besenski N. Traumatic injuries: Imaging of head injuries. EurRadiol 12:1237, 2002

2. National Institute for Health and Clinical Excellence: Headinjury: triage, assessment, investigation and early managementof head injury in infants, children and adults. Available at:http://www.nice.org.uk/nicemedia/pdf/CG56NICEGuideline.pdf.Accessed May 15, 2008

3. Go JL, Vu VN, Lee KJ, et al: Orbital trauma. Neuroimaging ClinN Am 12:311, 2002

4. Zee CS, Go JL: CT of head trauma. Neuroimaging Clin N Am8:525, 1998

5. Kratky V, Hurwitz J, Avram D: Orbital compartment syndrome.Direct measurement of orbital tissue pressure: 1. Technique.Can J Ophthalmol 25:293, 1990

6. Li J, Herndon LW, Asrani SG, et al: Clinical comparison of theProview eye pressure monitor with the Goldmann applanationtonometer and the Tonopen. Arch Ophthalmol. 122:1117, 2004

7. Vladimer K, Hurwitz J, Avram D: Orbital compartment syn-drome. Direct measurement of orbital tissue pressure: 1. Tech-nique. Can J Ophthalmol 25:293, 1990

8. Philips BB: Traumatic disorders, in Crenshaw AH (ed): Cam-bell’s Operative Oethopaedics (6th ed). St Louis, MO: MosbyYearbook, 1992, chap 38

9. Fuller DG, Hutton WL: Prediction of postoperative vision ineyes with severe trauma. Retina 10(Suppl 1):S20, 1990

0. Pieramici DJ, Au Eong KG, Sternberg P Jr, et al: The prognosticsignificance of a system for classifying mechanical injuries ofthe eye (globe) in open-globe injuries. J Trauma Injury InfectCriti Care 54:750, 2003

1. Cornelius CP, Altenmuller E, Ehrenfeld M: The use of flashvisual evoked potentials in the early diagnosis of suspectedoptic nerve lesions due to craniofacial trauma. J Craniomaxil-lofac Surg 24:1, 1996

2. Yuksel A, Sarslan O, Devranoglu K: Effect of valproate andcarbamazepine on visual evoked potentials in children. ActaPaediatr Jpn 37:358, 1995

3. Gellrich NC, Zerfowski M, Eufinger H, et al: A new diagnosticschedule and reliable treatment plan for traumatic optic nervelesions. Mund Kiefer Gesichts Chir 2(Suppl 1):107, 1998

4. Ikejiri M, Adachi-Usami E, Mizota A, et al: Pattern VE potentials intraumatic optic neuropathy. Ophthalmologica 216:415, 2002

5. Mahapatra AK, Bhatia R: Predictive value of visual evokedpotentials in unilateral optic nerve injury. Surg Neurol 31:339,1989

6. Goodall KL, Brahma A, Bates A, et al: Lateral canthotomy andinferior cantholysis: An effective method of urgent orbital de-compression for sight threatening acute retrobulbar haemor-rhage. Injury 30:485, 1999

7. Zacharides N, Papavassiliou D, Christopoulos P: Blindness afterfacial trauma. Oral Surg Oral Med Oral Pathol Oral RadiolEndod 81:34, 1996

8. Hislop WS, Dutton GN: Retrobulbar haemorrhage: Can blind-ness be prevented? Injury 25:663, 1994

9. Edwards P, Arango M, Balica L, et al: CRASH trial collaborators.Final results of MRC CRASH, a randomised placebo-controlledtrial of intravenous corticosteroid in adults with head injury-outcomes at 6 months. Lancet 365:1957, 2005

0. Spoor TC: An Atlas of Ophthalmic Trauma. London, MartinDuntz Publishing, 1997

5

5

5

5

5

5

5

5

5

6

6

6

6

1920 ACUTE PROPTOSIS IN TRAUMA

1. Saussez S, Choufani G, Brutus J, et al: Lateral cantho-tomy; A simple and safe procedure for orbital haemorrhagesecondary to endoscopic sinus surgery. Rhinology 36:37,1998

2. Vassallo S, Hartstein M, Howard D, et al: Traumatic retrobulbarhemorrhage: Emergent decompression by lateral canthotomyand cantholysis. J Emerg Med 22:251, 2002

3. Graham SM, Carter KD: Combined-approach orbital decom-pression for thyroid-related orbitopathy. Clin Otolaryngol Al-lied Sci 24:109, 1999

4. Chestnut RM, Marshall LF, Klauber MR: The role of secondarybrain injury in determining outcome from severe head injury.J Trauma 34:216, 1993

5. Fernside MR, Cook RJ, McDougall P, et al: The Westmead HeadInjury Project Outcome in severe head injury. A comparativeanalysis of pre-hospital, clinical, and CT variables. Br J Neuro-surg 7:267, 1993

6. Asensio JA, Forno W, Castillo G, et al: Posterior ischemic opticneuropathy related to profound shock after penetrating thora-

coabdominal trauma. South Med J 95:1053, 2002

7. Basile C, Addabbo G, Montanaro A: Anterior ischemic opticneuropathy and dialysis: Role of hypotension and anemia. JNephrol 14:420, 2001

8. Chang SH, Miller NR: The incidence of vision loss due toperioperative ischemic optic neuropathy associated with spinesurgery: The Johns Hopkins Hospital Experience. Spine 30:1299, 2005

9. Jackson TL, Farmer CK, Kingswood C, et al: Hypotensive isch-emic optic neuropathy and peritoneal dialysis. Am J Ophthal-mol 128:109, 1999

0. Remigio D, Wertenbaker C: Post-operative bilateral vision loss.Survey Ophthalmol 44:426, 2000

1. Rupp-Montpetit K, Moody ML: Visual loss as a complication ofnonophthalmologic surgery: A review of the literature. AANA J72:285, 2004

2. Slavin ML: Ischemic optic neuropathy after cardiac arrest. Am JOphthalmol 104:435, 1987

3. Suzuki D, Ilsen PF: Hypovolemic ischemic optic neuropathy.

Optometry 71:501, 2000