Download small series of patients, FA leakage

Table 3. CNV Lesion Size
and Last FA Results
Total Area
of CNV, mm2
Patient
Baseline
Last
Last FA
1
2
3
4
5
0.99
0.26
0.82
0.19
0.88
0.99
0.21
0.68
0.16
0.87
Min
No
Min
No
Min
Abbreviations: CNV, choroidal
neovascularization; FA, fluorescein angiography;
Min, leakage size less than 50% of the area
found at baseline; No, no leakage.
corrected VA (BCVA) at baseline
ranged from 10/160 to 10/16. Baseline BCVA in patient 1 was 10/50 and
reached a value of 10/16 3 months
later. At the beginning of the study,
patients 2 and 5 (treated with PDT)
had BCVAs of 10/160 and 10/100,
respectively. One week after IVB injection, their BCVAs increased to 10/
100 and 10/25, respectively, and this
result was stable up to the end of follow-up. One week after the injection, the BCVA of patient 3 increased from 10/32 to 10/22; at the
end of the follow-up (6 months), his
BCVA further improved to 10/16.
The BCVA of patient 4 quickly improved from 10/16 to 10/10. This patient was monitored for 9 months,
and at the last follow-up check, his
BCVA was 10/12.5 (Table 2).
Angiographic examinations
showed a decreased CNV leakage in
all patients, whereas the CNV size did
not show significant variation over
the follow-up period (Table 3).
Lastly, neither systemic nor local adverse effects were reported following IVB injection.
Comment. Current available laser
treatments for CNV secondary to AS
have a poor outcome. This might be
because of the high angiogenic activity present in CNV, which could
be worsened by the VEGF stimulation and up-regulation induced by
the treatment itself.5 These data support IVB use in the management of
CNV due to AS. In our experience,
IVB injection did not modify the
CNV size, whereas an increase in final lesion size in CNV due to AS has
been reported after PDT.2 In our
small series of patients, FA leakage
diminished in patients 1, 3, and 5
and was completely absent in patients 2 and 4. A reduction of CRT
was recorded in all subjects. This
change of retinal morphology is
likely to be the result of a combined antiexudative effect due to the
decrease of vessel permeability and
the antiproliferative effect due to the
inhibition of further CNV growth
following the VEGF blockage.5 The
smallest reduction was recorded in
the 2 patients who had previously
undergone PDT. These anatomical
improvements were associated with
concomitant increases in VA (a mean
of 3-4 lines). The mechanism of this
outcome remains uncertain.
A previous case report of CNV
due to AS treated with IVB by
Teixeira and coworkers4 shows an
improvement of the patient’s BCVA.
Posttreatment optical coherence tomography and FA imaging showed
no presence of subsensory fluid or
leakage, respectively. Our data seem
to confirm the efficacy and safety of
anti-VEGF therapy in eyes with CNV
secondary to AS, although we realize that the present study has some
limitations, including the limited
number of patients and the short period of follow-up. Nevertheless, considering the relative rarity of the disease, it would be difficult to conduct
randomized controlled trials, which
require a higher number of patients with CNV secondary to AS.
Michele Rinaldi, MD
Roberto dell’Omo, MD
Mario R. Romano, MD
Flavia Chiosi, MD
Ugo Cipollone, MD
Ciro Costagliola, MD
Correspondence: Dr Costagliola, Dipartimento di Scienze per la Salute,
Università degli Studi del Molise, Via
Francesco De Sanctis s.n.c., 86100
Campobasso, Italy (ciro.costagliola
@unimol.it).
Financial Disclosure: None reported.
1. Gass JDM. Angioid Streaks: Stereoscopic Atlas of
Macular Diseases. St Louis, MO: Mosby; 1997:
118-123.
2. Menchini U, Virgili G, Varano M, et al. Outcome of choroidal neovascularization in angioid streaks after photodynamic therapy. Retina.
2004;24(5):763-771.
3. Rich RM, Rosenfeld PJ, Puliafito CA, et al. Shortterm safety and efficacy of intravitreal bevaci-
(REPRINTED) ARCH OPHTHALMOL / VOL 125 (NO. 10), OCT 2007
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zumab (Avastin) for neovascular age-related
macular degeneration. Retina. 2006;26(5):
495-511.
4. Teixeira A, Moraes N, Farah ME, Bonomo PP.
Choroidal neovascularization treated with intravitreal bevacizumab (Avastin) in angioid
streaks. Acta Ophthalmol Scand. 2006;84(6):
835-836.
5. Gomi F, Nishida K, Oshima Y, et al. Intravitreal
bevacizumab for idiopathic choroidal neovascularization after previous injection with posterior subtenon triamcinolone. Am J Ophthalmol.
2007;143(3):507-509.
Laser In Situ Keratomileusis
Flap Necrosis After
Trigeminal Nerve Palsy
Laser in situ keratomileusis (LASIK)
surgery can induce changes in the
corneal epithelium owing to a neurotrophic phenomenon as a consequence of the sectioning of nerves
during flap cutting. 1 More profound alterations have been reported with a superior hinge, compared with a nasal hinge, and the
associated effects tend to normalize over approximately 6 months,2
although it is possible that complete reinnervation and recovery of
the basal state may not occur.3 Epithelial damage has also been associated with a reduced blinking rate,
which favors corneal exposition.4
To date, various cases of postLASIK neurotrophic epitheliopathy have been reported, characterized by symptoms and signs of dry
eye and a spotted distribution of rose
bengal dye. Recommended treatments include artificial tears, tear
plug, and autologous serum,5 among
others. Herein, we report a case of
severe corneal flap necrosis that occurred after formation of a trigeminal nerve lesion of vascular origin.
The patient was successfully treated
with autologous plasma rich in
growth factors (PRGF).6
Report of a Case. A male patient,
48 years old and a smoker, underwent LASIK surgery of both eyes in
2000 for myopia (−5.00 OD and
−6.00 OS). A microkeratome (Hansatome; Bausch & Lomb, Rochester, New York) was used to produce a cut with a diameter of 8.5
mm and a depth of 160 µm. Postoperative evolution was without
incident, and the patient demonstrated satisfactory visual and clinical recuperation.
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In December 2003, the patient
arrived at the accident and emergency service of a local general hospital with what appeared to be a leftsided cerebrovascular injury, which
was confirmed on brain computed
tomographic scan. The same scan revealed several areas of small lacu-
nar infarctions, one of them affecting the deep area of the right medial
cerebral artery, for which the patient was asymptomatic. He was hospitalized for 5 days.
In May 2004, as a result of visual loss in his left eye in the absence of pain, the patient consulted
Figure 1. Flap necrosis at the inferior edge of the laser in situ keratomileusis flap.
his ophthalmologist, who observed
flap necrosis at the inferior edge
(Figure 1). Lubricant treatment was
initiated, and because of poor evolution, the patient was referred to our
center for further treatment. At that
stage, he had necrosis of the temporal half of the flap associated with anesthesia of the left trigeminal region. The patient was treated
successively during the following
weeks with artificial tears without
preservatives, tear plug, autologous plasma, cyanoacrylate adhesive, amniotic membrane patch, and
a bandage contact lens. Two months
later, epithelialization was achieved,
leaving as a consequence an anterior stromal opacity and notable topographic irregularity (Figure 2),
which only permitted a bestcorrected visual acuity of less than
20/200, as measured with eyeglasses.
To improve corneal irregularity,
we proceeded in October 2005 to extirpate the flap remnant and apply
temporal tarsorrhaphy together with
3 layers of amniotic membrane to increase the permanence period, together with temporal tarsorrhaphy.
Despite this procedure, an exten-
Figure 2. Orbscan (Bausch & Lomb, Rochester, New York) showing the corneal irregularity after partial flap necrosis.
(REPRINTED) ARCH OPHTHALMOL / VOL 125 (NO. 10), OCT 2007
1424
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eye to respond to certain situations
that involve aggression to the ocular
surface. Without ruling out the possibility that the trigeminal lesion may
have caused a corneal ulcer, this patient demonstrated flap necrosis with
minimum repercussion in the deep
corneal layers. On removal of the flap
remains and despite measures to favor reepithelialization, signs of wound
healing were not apparent. In light of
this poor response and the risk of corneal melting, treatment with PRGF
was initiated. This treatment has been
used previously in maxillofacial and
orthopedic surgery. Treatment with
PRGF involves obtaining platelet and
plasma proteins from the patient. The
extract contains a high concentration of growth factors that can enhance the mechanisms of repair and
regeneration in distinct tissues.6 It is
prepared by centrifuging a sample of
the patient’s blood and obtaining a
plasma fraction enriched in platelets
from which growth factors are released with the addition of calcium
chloride. This treatment is being used
in other patients with different forms
of neurotrophic keratitis and is being
subjected to further evaluation to
characterize its efficacy.
Figure 3. Epithelial defect after the amniotic membrane dissolution (lissamine green).
Germa´n A. Rocha, MD
Arantxa Acera, DSc
Juan A. Dura´n, MD
Correspondence: Dr Dura´n, Instituto Clı´nico-Quiru´rgico de Oftalmologı´a, Virgen de Begon˜a 34, 48006
Bilbao, Spain ([email protected]).
Financial Disclosure: None reported.
Figure 4. Improvement of the epithelial defect after treatment with autologous plasma rich in growth
factors.
sive epithelial defect in the resected zone persisted 1 month later
(Figure 3). Consequently, in December 2005 and with the informed consent of the patient, we decided to commence treatment with
PRGF (GAC Medical, Vitoria,
Spain). Initially, approximately 20
µL (1 drop) was administered every 2 hours, progressively reducing
the frequency of administration in
accord with the observed improvement. During the following 6 weeks,
progressive epithelial closure was observed (Figure 4), although long-
term irregularity of the epithelium
and opacity of the underlying stroma
persisted. The final best-corrected visual acuity was 20/200.
Comment. This case presents 2 particularly salient aspects. First, we report flap necrosis due to a trigeminal nerve lesion more than 3 years
after LASIK surgery. Second, we describe a novel method for the successful treatment of neurotrophic
ulcers.
The first aspect raises doubts about
the capacity of a LASIK-operated on
(REPRINTED) ARCH OPHTHALMOL / VOL 125 (NO. 10), OCT 2007
1425
1. Wilson SE, Ambro´sio R. Laser in situ keratomileusis–induced neurotrophic epitheliopathy. Am
J Ophthalmol. 2001;132(3):405-406.
2. Donnenfeld ED, Solomon K, Perry HD, et al.
The effect of hinge position on corneal sensation and dry eye after LASIK. Ophthalmology.
2003;110(5):1023-1029.
3. Calvillo MP, McLaren JW, Hodge DO, Bourne
WM. Corneal reinnervation after LASIK: prospective 3-year longitudinal study. Invest Ophthalmol Vis Sci. 2004;45(11):3991-3996.
4. Savini G, Barboni P, Zanini M, Tseng SCG.
Ocular surface changes in laser in situ keratomileusis–induced neurotrophic epitheliopathy
[published correction appears in J Refract Surg.
2005;21(1):10]. J Refract Surg. 2004;20(6):
803-809.
5. Fuchsluger TA, Steuhl K, Meller D. Neurotrophic keratopathy: a post-LASIK case report
[in German]. Klin Monatsbl Augenheilkd. 2005;
222(11):901-904.
6. Anitua E, Andia I, Ardanza B, Nurden P, Nurden AT. Autologous platelets as a source of protein for healing and tissue regeneration. Thromb
Haemost. 2004;91(1):4-15.
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