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1026
Figure 1 (A) Pigmented posterior vitreous cyst,
free floating in the posterior segment. (B) B scan
ultrasound demonstrating the posterior vitreous
cyst measuring 5.4 mm in diameter. The
posterior hyaloid face was intact.
vascular system.34 The presence of blood vessels in some cases, and their proximity to
Cloquet's canal, gave support to this hypothesis. However, some cysts are neither vascularised nor are they attached to, or located near,
Cloquet's canal. In a review of the literature,
Francois reported five vascularised cysts out
of nine.5 Hilsdorf, in a further review of 34
cases of vitreous cysts, found 11 to be anterior
cysts, and of the posteriorly situated cysts
seven were found in association with retinitis
pigmentosa and two with optic atrophy.6
Feman and Straatsma in a report of a case in
Letters
which the cyst was mobile within a small cavity in the posterior vitreous overlying the optic
nerve and macula, highlighted the controversy
over their pathogenesis.7 Orellana and colleagues reported on the microscopic appearance of a free floating vitreous cyst with its
wall made up of a layer of heavily pigmented
cuboidal cells, intermingled with nonpigmented cells, forming papillae. Electron
microscopy showed the lining cells to contain
mature and immature melanosomes, polarised basement membrane, and apical microvilli.' These findings support the hypothesis
that the cysts originate from the pigmented
ciliary epithelium and that trauma may play a
role in their development. Awan, however,
reported a history of trauma in only 2.7% of
cases.8
The likelihood is that vitreous cysts originate from different intraocular structures, the
vascularised, attached cysts from hyaloid
vascular remnants and pigmented, free floating cysts from the ciliary body epithelium.
Although the majority are asymptomatic,
troublesome symptoms can arise when they
float across the visual axis or come within its
vicinity. In the case reported, the onset of
symptoms may have been associated with
increased mobility of the cyst due to liquefaction of the surrounding vitreous gel or partial
posterior vitreous detachment.
The severity of symptoms occasionally warrants treatment. Surgical excision through the
pars plana has been reported,' but there is
potential for serious complications from this
approach. Argon laser photocystotomy offers
an alternative to surgical treatment,2 but its
effectiveness depends on the presence of
extensive pigment in the cyst wall and there is
a risk of inadvertent retinal photocoagulation.
Neodymium-YAG laser has previously been
used for the treatment of persistent subinternal limiting membrane and posterior hyaloid
face haemorrhages, vitreous floaters, vitreous
adhesions, and for the lysis of vitreous
bands.910 In the case described, Nd-YAG laser
was effective in disrupting the wall of a posterior vitreous cyst. Although the cyst did not
disappear completely, disruption of the cyst
wall caused a reduction in its size. In addition,
the cyst wall, being denser than the surrounding liquefied vitreous, gravitated out of the
visual axis with relief of symptoms.
In conclusion, vitreous cysts, though rare,
can give rise to intractable visual symptoms.
Surgical treatment is hazardous and argon
laser photocystotomy may not be effective. We
report the successful treatment of a posterior
vitreous cyst by Nd-YAG laser photocystotomy.
5 Francois J. Pre-papillary cyst developed from
remnants of the hyaloid artery. BrJ7 Ophthalmol
1950;34:365-8.
6 Hilsdorf C. Uber einen Fall einer einseitigen
Glaskorpercyste. Ophthalmologica 1965;149:1220.
7 Feman SS, Straatsma BR. Cyst of the posterior
vitreous. Arch Ophthalmol 1974;91:328-9.
8 Awan KJ. Multiple free floating vitreous cysts
with congenital nystagmus and esotropia. J Paediatr Ophthalmol 1975;12:49-53.
9 Raymond LA. Neodymium:YAG laser treatment
for haemorrhages under the internal limiting
membrane and posterior hyaloid face in the
macula. Ophthalmology 1995;102:406-11.
10 Tsai WF, Chen YC, Su CY. Treatnent of
vitreous floaters with neodymium YAG laser. Br
J Ophthalmol 1993;77:485-8.
Sudden unilateral visual loss and brain
infarction after autologous fat injection
into nasolabial groove
EDIrOR,-Central retinal artery occlusion
(CRAO) following cosmetic surgery seems to
be a very rare and devastating disease
inducing sudden visual loss. Even if vigorous
and massive treatment is advocated initially,
the prognosis of visual recovery is very disappointing.
In this paper, we report one case of CRAO
combined with brain infarction resulting from
an autologous fat injection for cosmetic problems.
We confirmed CRAO by fluorescein angiography and brain infarction by magnetic resonance imaging (MRI) and four vessel angiography.
To our knowledge, there have been no
reports of CRAO combined with brain infarction in autologous fat injection procedures.
This case gives a warning to cosmetic plastic surgeons and ophthalmologists of the
importance of careful manipulation and immediate awareness and treatment of iatrogenically induced ocular complications.
CASE REPORT
A 42-year-old woman came to the emergency
room in an irritated state. Two hours earlier,
The authors thank Ms M Restori for carrying out the
ultrasound examination.
H TABANDEH
P J ALLEN
P K LEAVER
Moorfields Eye Hospital, London
Correspondence to: H Tabandeh, Moorfields Eye
Hospital, London EC1V 2PD.
Accepted for publication 28 June 1996
Figure 2 (A) Posterior vitreous cyst shrank and
gravitated immediately after YAG laser
photocystotomy. (B) B scan ultrasound following
YAG laser photocystotomy, demonstrating a
reduction in size to 1. 6 x 2.2 mm (borders
delineated by the measuring calipers).
1 Orellana J, O'Malley RE, McPherson AR, Font
RL. Pigmented free floating vitreous cysts in two
young adults: electron microscopic observations. Ophthalmology 1985;92:297-302.
2 Awan KJ. Biomicroscopy and argon laser photocystotomy offree floating vitreous cyst. Ophthalmology 1985;92:1710-11.
3 Duke-Elder S. System of ophthalmology. Vol 2.
London: Henry Kimpton, 1964:763-4.
4 Elkington AR, Watson DM. Mobile vitreous
cysts. BrJ Ophthalmol 1974;58: 103-4.
Figure 1 (A) The fundal appearance 12 hours
after autologous fat injection shows multiple fat
emboli in the central retinal artery and vein.
Oedematous retina and cherry red spot are also
seen. (B) The fundus of the same patient taken
3 months after fat injection shows an atrophic
optic nerve and thick fibrous membranes on the
posterior pole.
Downloaded from http://bjo.bmj.com/ on June 17, 2017 - Published by group.bmj.com
1027
Letters
the left eye had a thick fibrous membrane on
the posterior pole and optic atrophy (Fig 1B).
COMMENrT
There are several articles reporting iatrogenic
CRAO caused by retrobulbar corticosteroid
injection,' talc emboli in an intravenous drug
abuse patient,' intranasal injection of corticosteroid for allergic rhinitis,' injection of lignocaine for rhinoplasty,4 and autologous fat
injection into the glabellar region.5 However,
it is debatable how the iatrogenically injected
materials emerged in the retinal circulation.
Some authors explained that the material was
injected directly into a branch of the ophthalmic artery and vascular disturbances occurred
because of retrograde flow of an intra-arterial
injection into the central retinal artery.`' In
this case, we assumed that CRAO had
developed as a result of a similar mechanism,
but unlike the other cases, it was accompanied
by brain infarction due to the fat embolism of
the branches of the cerebral artery. It is possible that the injection forces were strong
enough to reach into the internal carotid
artery, so a fat embolism occurred both at a
branch of the ophthalmic artery and at a
branch of the cerebral artery.
In the treatment of CRAO, no consensus
currently exists regarding therapy.6 Schmidt et
al 7 supported the theory that emboli resulting
from lipid, cholesterol, and calcific emboli
cannot be expected to respond to thrombolytic therapy. The patient did not take the
thrombolytic agent, but received ocular massage and carbon dioxide and oxygen therapy
intermittently.
This peculiar case should be a warning to all
ophthalmologists and plastic surgeons that
widely performed simple procedures can
cause irreversible misery, and the risk of damage should be explained to the patient. If there
is any evidence of a visual problem, prompt
consultation with an ophthalmologist is
needed.
Figure 2 Four vessel angiography of the central retinal artery shows decreased calibre of the
ophthalmic artery (B, arrowhead) compared with the normal side (A, arrowhead). Ocular blush in
the ophthalmic artery is missing on the left side (D, arrow) compared with normal ocular blush on the
right side (C, arrow). MRI scanning of the brain shows the low signal intensities on Tl weighted
images in the left caudate head (E) and thalamus (G), compared with the high signal intensities on
T2 weighted images in the left caudate head (F, arrow) and thalamus (H, arrow).
she had undergone a fat transplantation of
abdominal fat to her nasolabial groove to correct a cosmetic problem. The procedure was
performed by a local plastic surgeon. Immediately after injection of autologous fat (0.5 ml)
mixed with blood and saline into her nasolabial groove, she complained of headache and
dyspnoea, became very irritable, and fell into
an almost unconscious state.
Physical examination in the emergency
room and enhanced brain computer tomography revealed no specific abnormalities.
Though the ocular examination had shown
abnormal pupillary reflex in the left eye, visual
acuity could not be checked owing to the
patient's general condition. The left pupil was
dilated about 8 mm and did not react to direct
light stimulus, but did react to indirect light
stimulus. Funduscopic examination showed
the typical appearance of CRAO with a cherry
red spot on the macula, and marked retinal
ischaemia and multiple emboli in retinal arte-
rioles (Fig IA). The patient was finally
diagnosed with CRAO due to autologous fat
emboli.
The laboratpry examinations were found to
be normal. Four vessel angiography revealed
that there was decreased calibre of the left
ophthalmic artery leading to ophthalmic
artery insufficiency (Fig 2A and B) and disappearance of the image of ocular blush (Fig 2C
and D) but there was no arteriovenous abnormality. The MRI showed multiple patched
high signal intensities in the left caudate head
(Fig 2E and F), thalamus (Fig 2G and H), and
subcortical white matter of the left cerebral
hemisphere.
The patient was treated with ocular massage and, intermittently, carbon dioxide and
oxygen therapy immediately. She recovered
her mental status in a week but lost her left
visual acuity. After 3 months, her ocular
condition was re-examined, but she had no
light perception in her left eye. The fundus of
DO HYUNG LEE
HAN NAM YANG
JAE CHAN KIM
KYUNG HWAN SHYN
Department of Ophthalmology, Chung-Ang University
Hospital, Seoul, Korea
Correspondence to: Kyung Hwan Shyn, MD,
Department of Ophthalmology, Chung-Ang University Hospital, 65-207 Han-gang ro 3 ga, Yong-san gu,
Seoul, Korea, 140-757
Accepted for publication 23 August 1996
1 Ellis PP. Occlusion of the central retinal artery
after retrobulbar corticosteroid injection Am J
Ophthalmol 1978;85:352-8.
2 Friberg TR, Gragiydas ES, Regan CDJ. Talc
emboli and macular ischemia in intravenous
drug abuse. Arch Ophthalmol 1979;97:105-9.
3 Whiteman DW, Rosen DA, Pinkkertonnn RMH.
Retinal and choroidal microvascular embolism
4
5
6
7
after intranasal corticosteroid injection. Am J
Ophthalmol 1980;89:851-3.
Cheney ML, Blair PA. Blindness as a complication of rhinoplasty. Arch Otolaryngol Head Neck
Surg 1987;113:768-9.
Derizen NG, Lisa F. Sudden unilateral visual loss
after autologous fat injection into the glabellar
area. Am J Ophthalmol 1989;107:85-7.
Kwaan H. Thromboembolic disorders of the eye
in thrombolytic therapy. In: Comerata AJ, ed.
Thrombolytic therapy. New York: Grune and
Stratton, 1988:-153-63
Schmidt D, Schumacher M, Wakhloo AK.
Microcathter urokinase infusion in central
retinal artery occlusion. Am J Ophthalmol 1992;
113:429-37.
Downloaded from http://bjo.bmj.com/ on June 17, 2017 - Published by group.bmj.com
Sudden unilateral visual loss and brain
infarction after autologous fat injection into
nasolabial groove.
D H Lee, H N Yang, J C Kim and K H Shyn
Br J Ophthalmol 1996 80: 1026-1027
doi: 10.1136/bjo.80.11.1026
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