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Visual Loss due to Orbital Fracture
The Role of Early Reduction
Alan F. Lipkin,MD; Gayle E. Woodson, MD;Robert H. Miller, MD
\s=b\Seriousinjuryto the optic nerveis an
uncommon, usually permanent, complica-ion of orbital fractures. Occasionally it is
due to reversible changes, such as ede-
ma, contusion, or compression of the
optic nerve. The early management ofvisual loss due to orbital fracture is con-
roversial. Some authors advocate emer-
gencyoptic nerve decompression; othersecommend steroid therapy alone. We
present a case of
nearly complete unilat-
eral loss of vision after a lateral orbital
racture with compression of the opticnerve by bony fragments. Computedomographic scanning of the orbit helpedusto pinpoint the cause of visual compro-mise and also served as a guide in plan-ning surgery. Large dosages of steroids,combined withearly reduction ofthe frac-
ure, resulted in substantial recovery ofvision. This case illustrates the impor-ance of preciselydetermining the nature
of the injury and the cause of visualcompromise. A protocol formanagement
of these injuries is presented.(Arch Otolaryngol Head Neck Surg
1987;113:81-83)
Eyeinjury seriousenough to resultin blindness has been estimatedto occur in 3% of facial fractures.1When blindness is immediate and
complete, theprognosis for even partial recovery is poor.23 Progressive orincomplete visual loss may be ameliorated either by large dosages of steroids or by emergency optic nerve
decompression, depending on the
mechanism of injury, the degree oftrauma to the optic canal, and theperiod of time that elapses betweeninjury and medical intervention.4
We recently treated a patient whosustained severe visual impairmentafter fracture of the lateral orbitalwall, optic canal, and zygoma. Computedtomography wasusedto help uslocalize the site of presumed opticnerve injury. Early reduction of thefractures, combined with large dosages of steroids, resulted in substantial recovery of vision.
REPORT OF A CASE
A 30-year-old man was brought viaambulanceto the Ben Taub GeneralHospital emergency room, Houston, after sustaining facial and headinjuries in a motorvehicle accident. His face had struck the
windshield, leading to a brief loss of consciousness and subsequent disorientation,confusion, and combativeness. On initialexamination, there were multiple facial
lacerationsandcompleteexternalophthal-moplegia on the left side. Chemosis and asmall subconjunctival hemorrhage werepresent. The pupil was 7 mm in diameterand nonreactive to light or accommodation.Thepatient was notsufficiently cooperative for visual acuity testing, but therewas noapparent response toconfrontationonthe leftside.Vision in the right eye wasnormal.
Computed tomographic(CT) scansof thehead and facial bones revealed amediallydisplacedfracture ofthe lateralwallof theleft orbit, with the fragment compressingto the optic nerve (Fig 1). Additionally,there were two fractures of the zygomaticarch, a fracture of the posterolateral wallof the sphenoidal sinus, and a fracture ofthesquamousportionof the temporalbonewith novisible brain injury. The patient'smental status cleared over a period ofseveral hours, and an ophthalmologicexamination was performed. The left eyecould only differentiate light and dark;there was not sufficient acuity to differentiate fingers or letters. There was no evidence of injury to the globe.
The patient was given an intravenousbolus of 10 mg of dexamethasone sodium
Accepted forpublication March 21, 1986.From the Departmentof Otorhinolaryngology
and Communicative Sciences, Baylor College ofMedicine, Houston. Dr Lipkin is now in privatepractice, Denver.
Presented in part at the Southern SectionalMeeting of the American Academy of FacialPlastic and Reconstructive Surgery, Orlando,Fla, Jan 18, 1986.
Reprint requests to Department of Otorhino-laryngology andCommunicativeSciences,BaylorCollegeof Medicine, 1 BaylorPlaza,Houston, TX77030 (Dr Woodson).
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Fig 1.Preoperative computed tomographic scan reveals mediallydisplaced fracture of left lateral orbital wall with bony fragmentcompressing optic nerve.
Fig 2.Postoperativecomputed tomographic scan reveals satisfactory reduction of orbital fractures.
Management of Orbital Fractures
No Injury to Vision
Reduction of Fractures
as Indicated
Complete Blindness
Steroids Only
Orbital Injury
Initial Stabilization
Head and Neck Evaluation
Ophthalmologic Evaluation
,
Facial Roentgenograms.
Visual Loss
4rComputed Tomographic Scans of Orbits and Face
Nerve Injury
Subtotal or Delayed Loss
Hematoma or
Fragments Injuring Nerve
ISteroids and Surgery
Ophthalmic Injury
Emergency Ophthalmologic Care
Later Reduction of Fractures
No Hematoma or
Fragments Injuring Nerve
Steroids
No Improvement ^ Improvement
Surgery
4
Fig 3.Our current management of orbital fractures.
phosphate and brought to surgery. Thefractures were reduced through a browincision andpreexistingfacial lacerations.The main fragment, which included thezygoma and lateral wall of the orbit, wasreduced only after the application of alarge amount of rotational force. The CTimages were used as aguide for the direction of motion in reducing andwiring thefractures.
Postoperatively, the patient was maintained on a course of dexamethasone sodiumphosphate (10 mgintravenously everysixhours), andthe dose was tapered over aten-day course. His vision and extraocularmotionsgraduallyimproved overthisperiod. After three days, he wasable to countfingers with the left eye, and after ten
days, he was able to read newsprint. Apostoperative CT scan (Fig 2) revealed
satisfactory reduction of the orbital fractures. One yearlater,the patienthas20/70vision in his left eye, normal motility, andan acceptable cosmetic result.
COMMENT
The globeand optic nerve arehighlyvulnerable to permanent injury afterbluntfacialtrauma.Hyphema,lens or
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etinal detachment, scierai rupture,nddamageto the nerve may all occurt the time of impact and lead toermanent visual loss. Injury to theptic nerve after facial fracture canccur anywhere along the course of
he nerve, but it is most commonwithinthebonyoptic canal.3Shearingorces after fractures can be
greatnough to transectthe nerve, leadingo immediate and irreversible blindess. Stretchinjuries to the nerve areotentially reversible, but they maye associated with intraneural orxtraneuralhematomasthat can com
ress the remaining viable neurons.n fact,injury to the nutrient vesselsfthe nervewithhemorrhageintotheheath,edema, and contusion may be
he most frequent mechanism ofisual loss.5 The centralretinalarterynd ophthalmic artery are seldomeriouslyinjured.Clinically, the timing and progres
ion of visual loss can be crucial in
etermining further treatment.lindnessoccurring at the moment of
njury carries a poor prognosis,egardless of treatment.5 Delayed orrogressive loss ofvisionimplies thatviable nerve isbeingcompressedby
dema or bleeding;in suchcases,earlyreatment may improve the prospector recovery. Theinjury canbe localzed using a combination of specialzedphysical andradiologie examinaons. Earlyophthalmologic consultaonis essentialin all casesof midfacer frontal injury.1 In addition to docu
mentation of visual acuity, majornjuries to the globe and adnexa cane excluded. Interpretation of plainoentgenograms may be difficultecause of superimposed soft-tissuewelling or bone artifact. Computed
omography allows the deeper struc-
tures of the orbit (including the opticnerve itself) and facial bones to bevisualizedwithunsurpassedaccuracy*and maybe used topinpointthe mostlikely areas of severe injury.It is generally agreed that initial
treatment should focus onthe overallstabilization of the patient, particu
larly in
ruling out head
injury that
may need urgent attention. Severeinjuries to the sclera, lens, or retinamay require emergency ophthalmicsurgery. Nonoperative interventionmay consist of administration ofpharmacologie doses of corticoste-roids (dexamethasone, up to 5 mg/kg/d) to reduce microcirculatoryspasm, edema, and nerve cell necrosis.1 The best results are achieved ifsteroids are given immediately afterinjury.
The role of surgeryafterinjuries tothe nerve iscontroversial,with therapeutic regimens in major centersranging from routine explorationafter all casesof traumaticvisual lossto never performing surgery. Hughes8found that, even in injuries thatdirectly involve the optic canal (only6% in his series), decompression ofthe nerve did not change the poorprognosis for recovery of usefulvision. His results arecontradictedbyseveral Japanese investigators910 whohave collectivelyperformed hundredsof transethmoidal optic nerve decompressions after trauma. In over 400operations performed by Pukado,10some improvement occurred in nearlyevery case, including those in whomthere was no initial light perceptionand those in whom months had
elapsed since their injuries. Andersonet al7 are more selectivein their useof
surgery, reserving itfor patients who
either (1) sustain delayed visual loss
that is unresponsive to 12 hours ofcorticosteroid therapy or (2) initiallyimprovewhilereceivingsteroidtherapy but then deteriorate, either whilereceivingsteroidtherapy orwhen itisbeing tapered. Although wegenerallyfavor this selective and pragmaticapproach, we feel that the results of
high-resolution CT scans
should alsobe considered whenmaking the decision about surgery. Fractures andhematomas can be precisely locatedpreoperatively, aiding the surgeon inapproaching areas of potentiallyreversible injury.
Our currentmanagement oforbitalfractures is as follows (Fig 3): Afterinitial stabilization and routine facial
roentgenograms, all patients areevaluated by both the otolaryngology andophthalmologyservices. If the injurydoesnotthreatenvision,the fracturesarereduced asindicated. If visionisatallcompromised, a high-resolutionCTscan of the orbits and facial boneswith soft-tissue and bone settings isobtained. Special effort is made tovisualize theoptic nerves and canals.High-dosage steroids are administered. If fragments significantlyimpinge on the nerve, CT images areused as a guide for relocation orremoval of the involved bone. Hema
toma is also a relative indication forimmediate surgery. In cases wherethere is no obvious impingement onthe nerve, steroids are given, and thepatient is carefully observed. If thepatient's vision deteriorates despitemedical treatment, the nerve isexplored anddecompressed. By treatingposttraumaticoptic nerve injuriesaggressively, usablevision can be preserved in a number of patients.
References
1. Holt GR, Holt JE: Incidence of eyeinjuries facial fractures: An analysis of 727 cases.
Otolaryngol Head NeckSurg1983;91:276-279.2. Maniglia AJ, Kronberg FG, Culbertson W:
isual loss associated with orbital and sinusseases. Laryngoscope1984;94:1050-1059.3. Manfredi SJ, Raji MR, Sprinkle PM, et al:
omputerized tomographic scan findings inacial fractures associated with blindness. Plast
econstrSurg 1981;68:479-490.4. Krausen AS, Ogura JH, Burde RM, et al:
Emergency orbital decompression: A reprievefrom blindness. Otolaryngol Head Neck Surg1981;89:252-256.
5. EdmundJ, Gottfriedsen E: Unilateral opticatrophy following head injury. ActaOphthalmol1963;41:693-697.
6. Grove AS: Computed tomography in themanagement of orbital trauma. Ophthalmology1982;89:433-440.
7. Anderson RL,Panje WR, Gross CE: Opticnerve blindness following blunt forehead trau-
ma. Ophthalmology1982;89:445-455.8. Hughes B: Indirect injury of the optic
nerves and chiasma. Bull Johns HopkinsHosp1962;111:98-126.
9. Niho S, Niho M, Niho K: Decompression oftheoptic canal by the transethmoidal route anddecompression of the superior orbital fissure.Can J Ophthalmol1970;5:22-40.
10. Fukado Y: Results in 400 cases of surgicaldecompression of the optic nerve. Mod ProblOphthalmol 1975;14:474-481.
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