Ophthalmology Volume 107, Number 5, May 2000

Table 1. Management of the Retinal Impact Site Without Surrounding Retinopexy After Intraocular Foreign Body Trauma

Patient No. Preop Macular

Age (yrs) Sex VA IOFB Type, Size Site of Retinal Impact VH Surgery (Time from Injury) ERM Postop VA Outcome
1. 33, M 20/30 Magnetic metal Superonasal, posterior ⫹ Vx (⬍ 24 hrs) ⫺ 20/20 at 8 yrs
2 ⫻ 2 ⫻ 1 mm to equator
2. 29, M HM Nonmagnetic metal 5 mm inferotemporal to ⫹⫹ Lx, Vx (⬍ 24 hrs) ⫺ 20/20 at 7 yrs
3 ⫻ 2 ⫻ 2 mm fovea
3. 14, M HM Magnetic metal 5 mm nasal to optic ⫹⫹⫹ Vx (⬍ 24 hrs) ⫺ Spontaneous PVD at 2
3 ⫻ 1 ⫻ 1 mm disc mos, 20/20 at 3 yrs,
20/40 at 10 yrs with
cataract
4. 50, M 20/30 Magnetic metal Superonasal, posterior ⫹ Lx, Vx (day 5) ⫺ Secondary IOL at 6 yrs,
4 ⫻ 1 ⫻ 1 mm to equator 20/20 at 8 yrs
5. 3, M LP Magnetic metal 5 mm superior to optic ⫹⫹ Lx, Vx (day 2) ⫺ Uncooperative with
2 ⫻ 1 ⫻ 1 mm disc amblyopia Rx, 4/200
at 9 yrs
6. 46, M HM Magnetic metal 2 mm temporal to fovea ⫹⫹ Lx, Vx (⬍ 24 hrs) ⫺ Spontaneous PVD at 1
4 ⫻ 2.5 ⫻ 1 mm wk, juxta- &
perifoveal CNM at 7
mos; Rx with laser;
perifoveal retinal
striae, 20/60 at 6 yrs
7. 23, M LP Nonretained pointed 8 mm superotemporal to ⫹⫹⫹ Repair of corneoscleral laceration ⫺ PVD at time of Lx, Vx,
metal fovea (⬍ 24 hrs) Lx, Vx (day 11) 20/20 at 16 mos
8. 36, M CF Metallic 4.5 ⫻ 2 ⫻ 2 3.5 mm inferior to optic ⫹⫹ Lx, Vx (⬍ 24 hrs) ⫺ Spontaneous partial PVD
mm disc at 6 mos with focal
vitreoretinal adhesion
at impact site,
perifoveal retinal
striae, 20/25 at 2 yrs
9. 3, M LP Nonretained tree Superotemporal, ⫹⫹ Lx, Vx (day 4) ⫺ 1/30 at 19 mos Patient
branch posterior to equator uncooperative with
amblyopic Rx
10. 22, M 20/ Magnetic metal 1 mm nasal to optic ⫹⫹ Lx, Vx (⬍ 24 hrs) ⫺ RRD (giant tear near
200 3 ⫻ 2 ⫻ 1 mm disc ora) at 3 mos (Vx,
SB), 20/20 at 1.5 yrs
11. 39, M LP Nonretained sheet 8 mm temporal to fovea ⫹⫹ Repair of corneoscleral laceration ⫹ 20/40 after cataract
metal and extending to ora (⬍ 24 hrs), which extended 8 surgery at 21 mos,
serrata mm posterior to limbus (no Vx macular ERM
or retinopexy) unchanged postop,
corneal astigmatism
12. 48, M 20/ Metallic 2 ⫻ 1 ⫻ 1 mm 3 mm nasal to optic ⫹ Vx, created PVD, unable to see ⫺ IOFB in posterior eye
400 (from CT scan) disc or remove IOFB with magnet wall on CT & US,
(⬍ 24 hrs) laser retinopexy for
small vitreous base
retinal tear at 1 mo,
20/20 at 9 mos

CF ⫽ counting fingers; CNM ⫽ choroidal neovascular membrane; CT ⫽ computed tomography; ERM ⫽ epiretinal membrane; HM ⫽ hand motions;
IOFB ⫽ intraocular foreign body; IOL ⫽ intraocular lens; LP ⫽ light perception; Lx ⫽ lensectomy; PVD ⫽ posterior vitreous detachment; RRD ⫽
rhegmatogenous retinal detachment; SB ⫽ scleral buckle; US ⫽ ultrasound; Vx ⫽ vitrectomy.
For vitreous hemorrhage (VH): mild (⫹) ⫽ view of optic disc and macula; moderate (⫹⫹) ⫽ view of peripheral retina in two or more quadrants but optic
disc and macula not visible; severe (⫹⫹⫹) ⫽ no retinal details seen.

7. Boscher-Southall C, Konqui P, Manderieux N, Pouliquen Y. Systemic Prednisolone Prevents Rebleeding in

Corps étrangers intra-oculaires. Techniques micro-chirurgi-
cales d’extraction et prévention du décollement de rétine: à
propos de 30 cas. J Fr Ophtalmol 1987;10:565–73.
8. L’Esperance FA Jr. Ophthalmic Lasers, 3rd ed. Vol. 2. St.
Louis: Mosby, 1989; 987.
9. Campochiaro PA, Bryan JA III, Conway BP, Jaccoma EH.
Intravitreal chemotactic and mitogenic activity. Implication of
blood-retinal barrier breakdown. Arch Ophthalmol 1986;104:
1685–7.
10. Jaccoma EH, Conway BP, Campochiaro PA. Cryotherapy
causes extensive breakdown of the blood-retinal barrier. A
comparison with argon laser photocoagulation. Arch Ophthal-
mol 1985;103:1728 –30.
Traumatic Hyphema
Dear Editor:
I read with interest the excellent report by Rahmani and
Jahadi (Ophthalmology 1999;106:375–9). We applaud and
thank them for including Yasuna’s systemic prednisolone
treatment.
I must first correct their literature review: They state
“Some studies have shown the beneficial effects of systemic
steroids . . . , while another failed to . . . ”. This “another”
study1 was refuted in my letter,2 which has been over-

812
 Letters to the Editor
Figure 1. Wallet-sized calling card TH Rx protocol that we have distrib-
uted to all residents (and at meetings). All residents were expected to carry
this card at all times when on duty and to implement it for all TH patients,
regardless of age. We credit this card with being responsible for our
excellent results reported in 1990.
looked. Yasuna’s protocol had not been well followed. Even
so, the rate of rebleeding was 50% greater in the control
group (steroids, 13%; control, 20%). They erred in statisti-
cal interpretation, incorrectly presuming failure to prove ⫽
disproved or proves the opposite.3 Rather, statistically there
was, in fact, a threefold greater probability that steroids
were beneficial than that they were not.
Second, Rahmani and Jahadi did not make a maximally
fair test of prednisolone because they did not completely
follow our recommended prednisolone regimen4 (see Fig 1)
regarding:
1. Testing for sickle cell anemia or trait
2. Full day’s dose of prednisolone, given as a loading
dose, “stat” immediately on diagnosis, in the eye
clinic or emergency department
3. Never dilate the pupil routinely or with short-acting
cycloplegics, only atropine and that, rarely
4. Absolutely no routine tonometry to avoid trauma
5. Instead they gave “topical timolol and oral acetazol-
amide . . . [for] . . . elevated IOP” [ⱖ21 mm Hg].
Such aggressive IOP management is neither medi-
cally necessary4 or desirable because it has several
real risks, especially in traumatic hyphema (TH).
Moreover, they state, “We were not able to show a
significant beneficial effect of oral prednisolone . . . ”. We
must strongly disagree with this conclusion. They, in fact,
did so. Their rebleeding rate was, steroids 18%; controls
26%. This is virtually identical to the previously refuted
1980 report,1 wherein the rebleeding rate was 50% greater
for the controls. Likewise, therefore, statistically, they can-
not say, or conclude, or announce, “no beneficial effect”
from steroids. Furthermore, a P ⫽ 0.21 on this difference
means the odds are four in five that you are really reducing
rebleeding and only one in five that it is luck or chance, a
fivefold probability that steroids are beneficial.
Therefore, there are no reports, to my knowledge, that
prove or even demonstrate that steroid therapy does not
reduce rebleeding, or is “not effective.” The only question is
how effective.
Regarding how effective steroids are, Farber et al5
showed that steroids are as effective (i.e., equally) as ami-
nocaproic acid (ACA). Moreover, Rahmani and Jahadi
found “Patients receiving prednisolone had a higher propor-
tion of secondary bleeding than did patients receiving [tran-
examic acid (TXA)] . . . but the difference was not statisti-
cally significant (P ⫽ 0.15)”. This is also compatible with
the hypothesis that prednisolone is as effective as TXA. (It
is possible that our resistance to unnecessarily testing for
and treating elevated intraocular pressure or dilating pupils
may also be partly responsible for our own still superior
results [Romano PE, Phillips P. No rebleeds in 48 consec-
utive cases of traumatic hyphema treated with systemic
corticosteroids. Presented as a poster at the Association for
Research and Vision in Ophthalmology, Sarasota, Florida,
May, 1988]).
Regarding their high rebleeding rate, I definitely agree
that it was because they did not use topical steroids (which
was done to avoid another confounding variable and for this
I commend them). I am absolutely convinced this is why TH
rebleeding rates have been decreasing because everyone
now gives topical steroids, and we have so stated in the
in-press fifth edition.4
Why don’t we then recommend topical steroids? Be-
cause our job is to, literally, be a nursemaid to a blood clot
for 5 days. Therefore, one must not unnecessarily touch or
otherwise traumatize the globe. We say “hands off”: no
tonometry, no drops etc., without a specific medical indica-
tion.
ACA and TXA prevent rebleeding, but so do systemic
steroids with an equally important, permanent, major role
because:
1. There remain medical situations in which ACA or
TXA are specifically contraindicated and steroids are
not.
2. There remain places where neither ACA or TXA may
be available (and steroids are).
3. ACA and TXA are too expensive, by fact or by third
party payer fiat.
4. The treating physician may, for fear of dangerous side
effects such as vomiting, prefer steroids.
5. The results of systemic steroids have, in our hands,
been superior to those reported for ACA and TXA.
Finally, regarding medical ethics in TH: There is no further
need for placebo-controlled studies in TH. No patient with
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 Ophthalmology Volume 107, Number 5, May 2000
TH should ever be again denied treatment with one of these
three agents.
PAUL E. ROMANO, MD, MSO
Dillon, Colorado
References
1. Spoor TC, Hammer M, Belloso H. Traumatic hyphema. Fail-
ure of steroids to alter its course: a double-blind prospective
study. Arch Ophthalmol 1980;98:116 –9.
2. Romano PE, Rynne MV. Traumatic hyphema [letter]. Arch
Ophthalmol 1981;99:2053– 4.
3. Kushner BJ. The use and abuse of statistics. [guest editorial].
Binocular Vision 1985;1:188 –90.
4. Romano PE. Traumatic hyphema. In: Fraunfelder FT, Ray FH,
eds. Current Ocular Therapy 4. Philadelphia: Saunders, 1995;
436 –9.
5. Farber MD, Fiscella R, Goldberg MF. Aminocaproic acid
versus prednisone for the treatment of traumatic hyphema. A
randomized clinical trial. Ophthalmology 1991;98:279 – 86.
Traumatic Optic Neuropathy
Dear Editor:
In “The Treatment of Traumatic Optic Neuropathy,” (Oph-
thalmology 1999;106:1268 –77), Levin et al reported that
there was no clear benefit for either corticosteroid therapy or
optic canal decompression surgery for traumatic optic neu-
ropathy (TON). The authors concluded from their results
and the literature review that although the number of pa-
tients studied was sufficient to exclude a major effect in the
treatment groups (untreated, corticosteroids, or optic nerve
decompression surgery), clinically relevant effects in spe-
cific subgroups could have been missed. The authors are to
be commended for their effort to try and bring an evidence-
based approach to the management of this most difficult
clinical problem.
It has been the practice at our institution (several of our
patients are included in the data set of this paper) to treat all
of our patients with acute, indirect TON with megadose
corticosteroids (methylprednisolone at dosages used in the
North American Spinal Cord Injury Studies1). Patients who
do not improve after a trial of megadose corticosteroids, can
not be weaned from steroids without visual loss, or who
have a surgically treatable lesion on a computed tomogra-
phy scan of the head (e.g., bone fragment impinging on the
optic nerve or optic nerve sheath hematoma) are offered
optic canal decompression surgery.2 We have tended to
offer the surgery more aggressively to patients with worse
vision (worse than 20/40 or more than 50% visual field loss)
with the idea that they have a more favorable risk-to-benefit
ratio (“less to lose and more to gain”).
We have not altered our clinical treatment of TON based
on the results of the study, but we do share the information
with the patients as part of the informed consent process.
Our rationale for treating all patients within these standard-
ized guidelines is that we have been unable to predict, based
on patient characteristics, mechanism of injury, duration of
injury, or severity of visual loss, who will benefit from
treatment and who will not. In addition, we have not en-
countered significant steroid-related side effects in our pa-
tients (typically young, previously healthy males) after
814
treatment with a short (48 –72 hour) course of megadose
steroids. I wonder if the authors would agree with our
approach and rationale based on the data and the literature.
Unfortunately, as the authors note, the most important
conclusions of the work are the need for a large, statistically
valid, randomized, controlled clinical trial for TON and the
persistent significant limitations and barriers for embarking
on such a trial.
ANDREW G. LEE, MD
Houston, Texas
References
1. Bracken MB, Shepard MJ, Collins WF, et al. A randomized,
controlled trial of methylprednisolone or naloxone in the treat-
ment of acute spinal-cord injury. Results of the Second Na-
tional Acute Spinal Cord Injury Study. N Engl J Med 1990;
322:1405–11.
2. Lee AG, Brazis PW. Clinical Pathways in Neuro-ophthalmol-
ogy: An Evidence-based Approach. New York: Thieme, 1998;
93–101.
Author’s reply
Dear Editor:
We appreciate Dr. Lee’s clear summary of the treatment
protocol he and his colleagues use for the treatment of acute
indirect TON. We agree that this approach is a reasonable
one, but also wish to point out that alternate approaches,
including no treatment, surgery, steroids alone, or various
combinations of these, are equally supported by the data
available in the literature, including our article. That is, the
best available evidence neither contradicts nor supports any
particular therapeutic plan, including that used by Dr. Lee.
Unfortunately (as discussed in our article), a randomized
controlled trial in this relatively uncommon disorder would
be difficult to carry out.
LEONARD A. LEVIN, MD, PHD
Roy W. Beck, MD
Michael P. Joseph, MD
Stuart Seiff, MD
Raymond Kraker, MSPH
for The International Optic
Nerve Trauma Study Group
Madison, Wisconsin
PRK for Myopia and Astigmatism
Dear Editor:
No data are offered in the paper by McDonald et al (Oph-
thalmology 1999;106:1481–9) to substantiate the assertions
that Autonomous Technologies Corporation LADARVision
excimer laser device “provides the technological platform to
effectively address corrections . . . [of] astigmatism” nor
that the “clinical results show the ATC LADARVision
excimer laser system is safe and effective for the reduction
of low-to-moderate myopia and astigmatism.” It is notable
also that the authors assertion is repeated in the “This Issue
At A Glance” section of the Journal. Visual acuity outcome
and sphere-equivalent data are provided on cases of myopic
astigmatism. However, neither simple nor vector analyses
of the toric ablation outcome are included, despite the stated
objective to assess the effectiveness of this device for astig-