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Case report
Central Retinal Artery Occlusion and Traumatic Optic Neuropathy Following Blunt
Ocular Trauma
‫صريللع ةيلإ دبرصإ تع نيارلا نيكبشا نالتعالا و نيكاملا نيكبشلا نايرش دادسنإ‬
Authors:
Jasmin Zvorničanin, MD,
Ferenc Kuhn, MD, PhD,
Meliha Halilbašić, MD, PhD,
Zlatko Mušanović, MD,
‫نؤفلؤملا‬
‫د‬. ‫نملاوانيواج نيمفاج‬
‫د‬. ‫نلوج كايريف‬
‫د‬. ‫جيؤاييلاح حيام‬
‫د‬. ‫حلميلكاح وكتالل‬
Authors affiliations:
Jasmin Zvorničanin, MD, Eye Clinic, University Clinical Center Tuzla, Trnovac bb, 75000
Tuzla, Bosnia and Herzegovina. Tel:38761134 874, E-mail:[email protected]
Ferenc Kuhn, MD, PhD, President, International Society of Ocular Trama Birmingham, AL,
USA; Research Director, Helen Keller Foundation Birmingham, AL, USA; Consultant
Zagorskiego Eye Klinik Krakow, Poland. Consultant Milos Eye Klinik Belgrade, Serbia;
Radoslava Grujića 25. Tel: 381112455759, E-mail: [email protected]
Meliha Halilbašić, MD, PhD, Eye Clinic, University Clinical Center Tuzla, Trnovac bb,
75000 Tuzla, Bosnia and Herzegovina. Tel: 38761728788, E-mail: [email protected]
Zlatko Mušanović, MD, Eye Clinic, University Clinical Center Tuzla, Trnovac bb, 75000
Tuzla, Bosnia and Herzegovina. Tel: 38761882601, E-mail: [email protected]
Corresponding author:
Jasmin Zvorničanin
Eye Clinic University Clinical Center Tuzla
Trnovac b.b., 75000 Tuzla, Bosnia and Herzegovina
Phone: +387 61 134 874; Fax: +387 35 250 474
E-mail: [email protected]
‫د‬. ‫نملاوانيواج نيمفاج‬
‫نؤيالا ضاحينو نؤيحا ملق‬
‫تلوك هعيحيب نؤطيا نؤفينا‬
‫نؤييراا نؤييلنا‬: ‫ب تيوميت‬.‫ب‬.،٧٥٠٠٠ ‫تلوك‬، ‫ضنؤهيمف نؤيلميا‬
‫نؤفياملا امق‬: ٣٨٧٦١١٣٤٨٧٤ ; ‫كينف‬: ٣٨٧٣٥٣٠٣٢٥٠
None of the authors has conflict of interest with the submission.
No financial support was received for this submission.
.‫نؤيلا ؤههن حيؤا دعق اا رافيتلن ضؤق نؤفصيؤم كا ترياب ؤارهق ؤاف نؤفلؤماج‬
Running title: Retinal Artery Occlusion and Traumatic Neuropathy
‫نؤنيالا نكعفالا ض نؤفيناا نؤنيالاب نيريا دولاند‬
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Abstract
A 15-year-old boy presented with a sudden loss of vision in his left eye immediately after
mild blunt facial trauma with the soccer ball. Clinical examination 1 hour after the injury
revealed visual acuity (VA) 20/20 in the right eye and no light perception (NLP) in the left
eye. Anterior segment of both eyes was unremarkable. Fundus examination in the left eye
presented diffusely pale retina with retinal vessel attenuation and no signs of retinal
hemorrhage. Fluorescein angiography performed one month after the trauma showed
restoration of central retinal flow and leakage around optic nerve head.
The patient was treated with conservative treatment for acute central retinal occlusion but the
VA maintained NLP. It is necessary for the ophthalmologist to keep in mind the possibility of
the trauma to cause central retinal artery occlusion and possibly traumatic optic neuropathy,
which may occur even in a case of mild facial trauma.
Key words: retinal artery occlusion, traumatic optic neuropathy, ocular trauma, blindness
‫ نؤيفي حج رييي ييا‬١٥ ‫نؤلنب عيع جيدم اياب ياحا هيا حيينيم نؤاليا عايب كا نؤيررا كا حمينم همتا اياأ عيحي‬
‫نؤتاا هاليم‬.‫نؤيصي جام ننمك نبييها هيا ضنجاو هليعا نؤليريا نؤملا‬٢٠/٢٠ ‫ؤيرلل نبدانا ضعاا نؤافيع نؤياج كا‬
‫نؤاليا نؤياج كا‬. ‫ميافا نيوك ؤيياياج نكحيحاا نؤريكا‬. ‫حم نؤياج نيالاا ؤتيق نيا نللب اضيم نؤاليا نؤياج ميق كلا‬
‫وارض هاضا ضؤالج نؤنيالاا اضعاا كا ييض‬. ‫علدو اضيم نكييها حج نهي هيا نؤميلاضماج هصيرا نؤنيالا نؤفصلري‬
‫ؤينيالاب نؤيصيا نؤتيا جلا ضعيعا تليرأ حم ؤينيالاا نؤفيناا نؤنيريا كا ةياياا هصلام نؤاا ميريا‬.
‫"ؤيرلل ددانا عاا" نكهصيا جاو نيك نؤليد نؤنيالا نؤنيريا ؤالولاند نؤفلملا نؤيالا حج نؤيلق عيع‬. ‫حج دوب‬
‫عج نؤييتح نؤنيالا نبأفالا نؤنيالا نؤنيريا تصاأ نؤفا نؤففيادو نكمييب نكعفييا كا رخأه اا نؤيالا ؤطياأ نؤريضاا‬
‫أمامب نيوك ضدا نؤلنب كا ضنؤييلو نؤالاحيا‬.
‫نؤيعالاا نؤاليفيا‬: ‫نؤفيناا نؤنيالا نؤنيريا نولاند‬، ‫نؤييلو عج نؤييتح نؤيصيرا ناعصيب نعفالا‬، ‫نؤياج ايلو‬
‫ضنؤيفع‬
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Introduction
Central retinal artery occlusion (CRAO) is an ophthalmic emergency with estimated incidence
of 10 in 1 million (1). There are only a few reported cases of retinal artery occlusion
following ocular contusion (2-7). Similarly, traumatic optic neuropathy (TON) is a rare cause
of severe permanent visual impairment following injury with estimated incidence of 1 in a
million (8). Combined CRAO and TON occur very rarely and have been reported in isolated
cases of ocular trauma (3, 6, 7).
We present a rare case of CRAO and TON with immediate visual loss following blunt facial
trauma with the soccer ball.
Case report
A 15-year-old boy was presented with a sudden loss of vision in his left eye immediately after
blunt facial trauma with the soccer ball. Clinical examination 1 hour after the injury revealed
visual acuity (VA) 20/20 in the right eye and no light perception (NLP) in the left eye. The
patient stated that he had sustained a minor hit by the ball in his left cheek where discrete skin
redness had been noted with no other signs of trauma. Anterior segment of both eyes was
unremarkable with measured intraocular pressure 15 mmHg. Fundus examination in the right
eye was normal and in the left eye it presented diffusely pale retina with retinal vessel
attenuation and no signs of retinal hemorrhage. The right pupil reacted normally to direct
light, while left pupil was unresponsive to light and showed an afferent pupillary defect.
Extraocular movements were full.
Next day in the morning, approximately twelve hours after the injury, the left eye fundus
showed formed cherry red spot in the fovea with significant diffuse retinal edema. Fundus,
color vision, visual field testing and visually evoked potentials (VEP) of the right eye were
normal. Ultrasonography (US) examinations of the eyeball and the optic nerve were normal in
both eyes. Optical coherence tomography (OCT) showed normal retina in the right eye and
severe retinal edema in the left one. Computed tomography (CT) and magnetic resonance
imagining (MRI) showed no signs of fractures nor optic nerve (ON) and brain abnormalities.
Color Doppler ultrasonography of heart, head and neck blood vessels were normal.
Neurologic and pediatric examinations were normal. Laboratory tests including inflammation
markers were within reference range. There was no evidence of any serious family diseases
and the patient’s twin brother is completely healthy.
The patient was treated with conservative treatment for acute CRAO including topical
mydriatics, steroids and acetazolamide orally, intravenous mannitol and methylprednisolone
1g for three days, following oral prednisone tapering for 4 weeks. Surgical options were
discussed but the parents declined. Ten days after the trauma, signs of retinal flow restoration
and retinal edema diminution were noted but the VA maintained unchanged. Fluorescein
angiography (FA) one month after the trauma was normal in the right eye, and in the left one
it showed restoration of central retinal flow, leakage around optic nerve head in all phases and
a small foveal leakage while arterial time was normal (Fig. 1). Final diagnosis of CRAO
complicated with TON was made.
Three months after the trauma, the VA in the left eye remained NLP, with normal anterior eye
segment, optic disc pallor and no signs of neovascularization development. OCT showed
small residues of retinal edema and significant reduction of retinal nerve fiber layer thickness
in the left eye.
Discussion
Retinal vascular occlusion is visually disabling, ocular vascular occlusive disorder associated
with arterial hypertension, diabetes mellitus, renal disease, ischemic heart and carotid artery
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disease (9). Trauma is a rare cause of isolated CRAO (4, 5), small branch vessel occlusions in
central and peripheral retina (2) and simultaneous CRAO and TON (3, 6, 7).
In this case, the clinical examination, US, OCT, FA and MRI did not find any signs of eye
perforation nor optic nerve avulsion (ONA). Severe retinal edema noted in the clinical
examination and OCT, with changes in retinal vasculature and “cherry red spot” indicate that
this is a case of CRAO. Unchanged VA after the retinal flow restoration and edema resolution
with noted leakage around the ON in FA one month after the injury all together indicate this is
also a case of TON.
The exact cause of the CRAO could not be determined in this case. The anatomy of the optic
nerve may explain how could a mild cheek blow result with such devastating eye injury.
There is no evidence of direct ocular trauma and the facial contusion probably induced
compression force which was transmitted to the orbit, which resulted in stretching of the
blood vessels. This could induce focal vasospasm and endothelium damage leading to
thrombus formation resulting in vessel occlusion and consequent retinal and ON ischemia (2).
The patient suffered complete loss of vision immediately after the trauma indicating that there
was also ON damage initially present and not only as a result of prolonged ischemia due to
vascular occlusion. There were no signs of bone fracture on CT scans nor ON damage or
edema on MRI and US, which suggest that this is a case of indirect TON and the ON was
probably damaged at the level of lamina cribrosa (1).
The management of CRAO includes non-invasive therapies with the aim to increase blood
oxygen content, dilate retinal arteries, dislodge emboli and increase central retinal artery
(CRA) perfusion. On the other hand, surgical options including anterior chamber paracentesis
or pars plana vitrectomy did not prove to be effective. Thrombolytics administered
intravenously or intra-arterially might also be a viable solution if applied as soon as possible
at most within 6 hours after CRAO. Conservative and thrombolytic therapy both have similar
significant outcomes (approximately 60%) with higher rate of adverse reactions associated
with thrombolytic approach (1). Equally, TON often results in severe visual loss and main
treatment options include systemic steroids and surgery in order to reduce ON swelling (10).
There is a relatively high rate of spontaneous visual recovery (57%) compared to steroids
(52%) and surgery (32%) in TON cases, showing that there are no convincing data that
steroids or surgical decompression of the optic nerve provide any additional visual benefit
over observation alone (10,11).
Out of three known cases of CRAO and TON two were treated with conservative and one
with operative treatment. In the first case CRAO was associated with ONA after direct ocular
trauma and the final VA was light perception (3). In the second case with direct ocular trauma
initial VA was NLP and maintained the same after the conservative therapy (6). Third case,
occurring after facial trauma, was initially treated with optic canal decompression and direct
ophthalmic fibrinolysis which resulted in VA improvement and respectable final VA of 6/9
(7). In our case, with mild facial trauma, the patient was treated with conservative treatment
and initial VA maintained NLP. Operative solutions were considered but it was not possible
due to financial limitations. Taking into account the results of research on CRAO and TON, it
can be concluded that each case has to be assessed on an individual basis. It is necessary to
recognize CRAO with possible TON on time and take all possible measures including
immediate surgery, otherwise VA prognosis is very poor.
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Fig. 1. A Fundus photography presenting optic nerve head pallor and residues of retinal
edema B. FA presenting restored central retinal flow, leakage around optic nerve head
Conclusion
We present a rare case of CRAO combined with TON as a result of mild head trauma,
resulting with complete and permanent visual loss in a young adult. This case highlights the
possibility of severe visual loss in a case of mild facial trauma and clinicians should be aware
of its potential devastating consequences.
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