Management of Traumatic Optic Neuropathy as a Part of Closed

Globe Injury : a Case Report

George Raden Mas Said1,2, Antonia Kartika1,2
1
Departement of Ophthalmology, Faculty of Medicine, Universitas Padjadjaran, Bandung,
Indonesia
2
National Eye Center, Cicendo Eye Hospital, Bandung, Indonesia

Abstract
Introduction: Closed Globe Injuries (CGI) are defined as injuries without full-thickness
defect to the cornea or sclera which can affect trauma from eyelid, anterior segment,
posterior segment, including optic nerve, resulting in traumatic optic neuropathy (TON).
Various management strategies have been investigated to give an appropriate treatment of
TON
Purpose: To report a case of visual improvement on traumatic optic neuropathy as a part of
closed globe injury
Case Report : A 30-year-old man presented with sudden vision loss and pain on the left eye.
Patient had history of blunt trauma two hours prior to admission to the hospital.
Ophthalmologic examination revealed visual acuity for the left eye was light perception
without projection. Direct and indirect of left eye’s light reflex was decreased and reverse
relative afferent pupillary defect was found on the right eye. Round, well-demarcated optic
disc in temporal region, berlin’s edema, hemorrage on vitreous, intraretinal, peripapil and
papillary was found from posterior segment examination. Patient was given various
medications in order to improve visual prognosis.
Conclusion : The approach to treating TON is a matter of debate, with no universally
agreed-upon timing for treatment. While some clinicians advocate for observation only,
others choose to intervene by administering systemic steroids, performing surgical
decompression of the optic canal, or employing both methods. Each case requires individual
assessment, and obtaining proper informed consent is crucial.
Keywords : Closed globe injury, traumatic optic neuropathy, visual improvement, visual
prognosis

I. Introduction
Closed globe injuries (CGIs) are defined as injuries without full-thickness defect
to the eyewall, which is cornea or sclera. Ocular trauma is one of the common causes
of ocular morbidity and visual impairment. There are no recent global estimates of
ocular trauma available in the literature. Estimates report close to 55 million ocular
injuries annually, of which 19 million loose vision or have a visual impairment.
Males are often at more risk because of more outdoor activities and risk-taking
behaviours. Closed globe injury can affect trauma from the eyelid, orbit, extraocular
muscles, anterior segment, posterior segment, including the optic nerve, resulting in
traumatic optic neuropathy.1,2,3

Traumatic optic neuropathy (TON) refers to any insult to the optic nerve
secondary to trauma. Motor vehicle and bicycle accidents are the most frequent
causes, accounting for 17% to 63% of cases. Loss of consciousness occurs in 40% to
72% of patients with traumatic optic neuropathy, and traumatic optic neuropathy
occurs in about 1.6% of head trauma cases and in 2.5% of patients with maxillofacial
trauma. It can be classified depending on the site of injury (optic nerve head,
intraorbital, intracanalicular or intracranial) or according to the mode of injury (direct
or indirect). Direct TON results from orbital or cerebral trauma that transgresses
normal tissue planes to disrupt the anatomical and functional integrity of the optic
nerve by avulsion of the nerve itself, from laceration by bone fragments or other
foreign bodies. Indirect TON is caused by the transmission of forces to the optic
nerve from a distant site without disruption of normal tissue structures. Normal tissue
planes are not transgressed in indirect TON. Instead, the anatomy and function of the
optic nerve are compromised by energy absorbed by the nerve at the moment of
impact. Little consensus exists regarding the appropriate treatment for TON. Various
management strategies have been investigated, including observation, corticosteroid
treatment, surgical decompression of the optic canal and combinations of steroids and
surgical decompression.1,4,5 This case presents a patient with traumatic optic
neuropathy as a part of closed globe injury and the management option provided.

II. Case Report

A 30-year-old male was admitted to the emergency room Cicendo Eye Hospital
with complained of blurry vision loss and pain in his left eye two hours prior. Patient
had history of blunt trauma by metal part of the rubber strap which being used to
fasten goods in motorcycle about 30 cm in front of the eye. He did not lose
consciousness, dizziness, or vomiting. The patient presented with bleeding and
hematoma from lower lid and redness in left eye. Initial examination revealed a stable
and alert patient. The vital sign is borderline with Visual Analogue Scale (VAS) score
seven out of ten.

Visual acuity for the right eye was 0.8 PH 1.0 with 16 mmHg in intraocular
pressure (IOP). The anterior segment examination was within normal limit, except for
the pupillary examination that showed the pupil was round, good direct and indirect
light reflex with positive reverse RAPD. The posterior segment of right eye revealed
round, well-demarcated optic disc, with Cup Disc Ratio (CDR) 0.3.

A B

Figure 1. Initial examination on patient. Swelling and vulnus

laceratum 4mm on palpebra inferior (A) Anterior
segmen of the patient (B).
Source : Cicendo Eye Hospital

Ophthalmologic examination for the left eye revealed visual acuity was light
perception without projection with 45 mmHg in IOP. There was vulnus laceratum
4mm and swelling in left lower palpebra, ciliary injection, corneal abration, corneal
edema. Anterior chamber depth revealed Van Herrick (VH) grade III with 1 mm
hifema, flare cell +4/+4. The pupil is mid dilatation, Light reflex was decreased. Left
eye posterior segment revealed well demarcated optic disc in temporal region, other
region unable to examine due to being covered by peripapillar hemorage. There was a
berlin’s edema and hemorrage in vitreous, intraretinal, peripapil and papil. Ishihara
color testing, amsler grid and contrast sensitivity on the right eye were within normal
limit while left eye were difficult to evaluate because of the limited visual acuity.
Ancillary examination was done on patient, revealed right eye optic nerve head
Optical Coherence Tomography (OCT) was within normal limit, while left eye optic
nerve head OCT had a low signal strength and showed an unreliable result.
Humphrey standard automated perimetry visual field testing (HVF) on right eye was
within normal limit while left eye showed a general depression visual field.

A B

C
B D E

Figure 2. Ancilary test in initial examination. Color fundus photography

on right (A) and left eye (B). Optic nerve head OCT (C), HVF
left eye (D) and HVF right eye (E)
Source : Cicendo Eye Hospital

The diagnosis of Closed Globe Injury Type Contusion Grade D Pupil (+) Zone III
OS + Susp. Traumatic Optic Neuropathy OS + Secondary Glaucoma OS + Vulnus
Laceratum Palpebra Inferior OS + Traumatic Iritis OS + Traumatic Iridoplegia OS +
Hyphema grade I OS + Corneal Abrasion OS + Berlin’s Edema OS + Vitreous
Hemorrage OS was made in view of the medical history and clinical findings.
Primary hecting on vulnus laceratum palpebra inferior left eye was done and he was
then started on a course of high dose intravenous methylprednisolone one gram/day
in four divided doses for three days. Other therapies that was given were omeprazole
40 miligram a day, citicoline 1000 gram a day, vitamin D3 1000 IU a day,
prednisolone acetate eye drop three times a day, cyclopentolate eye drop three times a
day, artificial tears eye drop six times a day, timolol maleate eye drop two times a
day, acetazolamide 250 miligrams three times a day, potassium chloride 600
miligrams a day.

Table 1. Patient progress during hospitalization

Source : Cicendo Eye Hospital

There was no adverse effect that occurred during treatment. His response to the
treatment is shown in Table I. There was an improvement in visual acuity on the first
and second day. The intraocular pressure decreased one day after the therapy, the
vulnus laceratum had been sutured. There was an improvement in posterior segment
condition, revealed a well-demarcated optic disc in temporal region, slight vitreous,
intraretinal, papil and peripapillary hemorrage and slight berlin's edema. Corneal
abrasion resolved on the third day. Ishihara colour test, amsler grid chard testing and
contrast sensitivity still difficult to assess. The fundus photograph was also performed
on the third day and the result was the improvement of posterior segment condition.

The diagnosis of Closed Globe Injury Type Contusion Grade D Pupil (+) Zone III
OS + Susp. Traumatic Optic Neuropathy OS + Traumatic Iritis OS + Traumatic
Iridoplegia OS + Hyphema grade I OS + Corneal Edema OS + Berlin’s Edema OS +
Vitreous Hemorrage OS was made due to the improvement of patient’s condition.
The patient was discharged on the third day and planned to visit the hospital in one
week to be followed up. The timolol maleate, acetazolamide, potassium chloride is
stopped being given due to the intraocular pressure decreased. Intravenous
methylprednisolone therapy replaced with oral methylprednisolone one milligram per
kilogram body weight, once daily for one week and tapered off after that.

Table 2. Patient progress during outpatient care

Source : Cicendo Eye Hospital

The next patient’s response to the treatment is shown in Table II. There was an
improvement in visual acuity on the 17th and 48th day. The anterior segment was
within normal limit on the 48th day, flare and cell were decreased by the time. There
were an improvement in posterior segment condition, revealed a round, well-
demarcated pale optic disc, minimal intraretinal hemorrage and subretinal fibrosis.
The patient could identify demoplate on day 17 th, 3/21 on 32nd day and 11/21 on 48th
day on Ishihara color testing while contras sensitivity was >25% on the 17 th day, 25%
on 32nd day and 1.25% on 48th day. There was no scotoma and metamorphosia on
amsler grid chard testing from the 17 th day and had a constant condition until the 48 th
day. The fundus photograph was also performed on the 32nd day and 48th day, the
result were the improvement of posterior segment condition. Ancillary examination
was done on patient on the 48th day, showed left eye optic nerve head OCT had a
papil atrophy on inferior and superior region. Humphrey standard automated
perimetry visual field testing (HVF) on right eye was within normal limit while left
eye showed a improvement in visual field. The diagnosis of Optic Atrophy OS post
Traumatic Optic Neuropathy + Intraretinal Hemorrage OS was made due to the
improvement of patient’s condition. The patient then continued methylprednisolone
tapered off and planned to had a correction spectacles for the next follow up.

Figure 3. Ancilary test. Color fundus photography left eye on initial

examination (A), third day of treatment (B), and 48 th day of
 treatment (C). OCT Papil (D), left eye HVF (E), and right eye
HVF on 48th day of treatment
Source : Cicendo Eye Hospital

III. Discussion
Closed globe injuries (CGIs) are defined as injuries without full-thickness defect
to the eyewall, that is, cornea or sclera. These are also referred to as nonpenetrating
injuries. Various classifications have been described to classify CGI. Standard
classification systems are essential to enable ophthalmologists to communicate
unambiguously by allowing standardization of terminology and also to enable
multicentre research. The most important of these are Birmingham Eye Trauma
Terminology (BETT) and Ocular Trauma Classification Group (OTC)1,2,4
Manifestation can affect Epithelial damage which can be abrasion, punctate
epithelial erosions, epithelial defect, foreign body due to breach in the epithelium and
revealed brilliantly on fluorescein staining. If the damage involves the pupillary axis,
the vision is grossly impaired. Corneal edema due to endothelial injury or extensive
damage due to abrasion. Corneal edema usually is associated with stromal edema,
and Descemet membrane (D.M.) folds. Accumulation of red blood cells within the
anterior chamber is referred to as a hyphema. A small amount of blood that is only
evident under close microscopic examination is referred to as a microhyphema. Blunt
trauma is the most common cause of a hyphema. Compressive force to the globe can
result in injury to the iris, ciliary body, trabecular meshwork, and their associated
vasculature. The shearing forces from the injury can tear these vessels and result in
the accumulation of red blood cells within the anterior chamber.1,2,5
Pupil examination can be found Traumatic mydriasis (iridoplegia) due to spasms
of the sphincter muscle, traumatic miosis occurs due to the irritation of ciliary
muscles and loss of accommodation. Pupillary margin rupture multiple sphincter tears
at the pupillary margin. Traumatic iritis is typically caused by blunt eye injury, In this
case, Traumatic iritis typically presents with unilateral ocular involvement in the
context of recent history of indirect blunt ocular trauma. It may present with white
blood cells and/or proteinaceous fluid in the anterior chamber; known as “cell and
flare” or “anterior chamber reaction”. Intractable secondary glaucoma may also result
following traumatic iritis. Topical cycloplegics (e.g. cyclopentalate 2% bid-tid,
scopolamine 0.25% bid) will dilate the pupil and prevent synechiae to the lens. They
also stabilize the blood-aqueous barrier to prevent further protein leakage (flare).
Topical cycloplegics will also prevent ciliary body and pupillary spasm that causes
pain and discomfort. Topical steroids (e.g. prednisolone acetate 1% qid) are used to
decrease inflammation. They are avoided if there is a corneal epithelial defect.
Topical beta-blockers (e.g. timolol maleate 0.5% bid) may be beneficial if secondary
glaucoma is present and there are no other contraindications to beta-blocker usage.1,3,5
Traumatic glaucoma is a type of secondary glaucoma that develops following
blunt or penetrating ocular trauma. This subtype of glaucoma usually entails several
mechanisms that interplay to produce increased intraocular pressure (IOP) and it is
important to consider all the pathophysiological mechanisms leading to increased IOP
as they influence management of patients.2,3,5
Posterior Segment Manifestations can have vitreous hemorrhage can be seen in
association with posterior vitreous detachment. vitreous hemorrhage is a relatively
common cause of acute vision loss. The three most common causes include;
proliferative diabetic retinopathy (PDR), posterior vitreous detachment (PVD) with or
without retinal tear, and ocular trauma, 59-88.5% of all cases. Patients are instructed
to minimize strenuous activity, as an increase in blood pressure may disrupt the newly
formed clot and cause new active bleeding. Patients are also instructed to keep their
head of bed elevated to allow settling of the blood, improving their vision and
permitting more complete fundoscopic examination. Bilateral patching and bedrest
may facilitate settling of blood. However, the patches must be removed immediately
before examination or treatment, as normal eye movements quickly disperse the
hemorrhage again. For this reason and its inconvenience to patients, bilateral
patching is infrequently attempted. Retinal hemorrhage can be flame-shaped or boat-
shaped. Flame-shaped hemorrhage occurs in cases with blunt trauma.3,5,6
Berlin's Edema (Commotio Retinae) usually presents as a cherry spot at the fovea
and results in milky white cloudiness at the posterior pole. Usually, berlin's edema
resolves on its own and, in some cases, may manifest as pigmentary changes at the
fovea. Retinal tear occurs in eyes predisposed to retinal tears like myopia, white
without pressure, or senile degeneration after blunt trauma. Montorio et al reported
OCTA findings over 6 months of 18 patients with Berlin's edema after blunt trauma;
an initial early decrease in vessel density in superficial and deep capillary plexuses
along with radial peripapillary capillary plexus was seen at 1 month with gradual
normalizing of the values at 6 months.2,4,6
Traumatic optic neuropathy can also result from blunt head or orbital trauma. The
patient usually presents with sudden vision loss, and there is RAPD with color vision
defect. Research in acute spinal cord trauma demonstrates that the pharmacologic
actions of very high doses of corticosteroids in this setting are separate and distinct
from the actions of steroids in the doses more typically encountered in clinical
practice. Experimental studies have demonstrated a biphasic dose response to
methylprednisolone in a range of doses much higher than the usual clinical usage.
There appears to be a distinct pharmacologic benefit of doses of methylprednisolone
in the range of 30 mg/kg—15 to 30 times the standard clinical dose.1,4,5
Traumatic optic neuropathy is a rare occurrence that leads to vision loss following
blunt or penetrating trauma to the orbitofacial region or head. Typically affecting
young males in their early thirties, this condition is commonly associated with
incidents such as motor vehicle accidents, bicycle accidents, falls, and assaults in
adults, while falls and road traffic accidents are more prevalent in pediatric cases.
When there's no penetration, traumatic optic neuropathy is often presumed to result
from an indirect injury, where the force of impact is transmitted to the optic nerve and
its blood vessels through soft tissues or bones. Notably, even relatively minor head
trauma can lead to indirect traumatic optic neuropathy..1,2,4,6-8
The patient in this case was a 30-years-old male complained of loss of vision and
pain in his left eye with history of blunt trauma. The gender, age and cause of TON
was suitable with epidemiological finding.
As mention in the case, the possibility of traumatic optic neuropathy should
always be considered in instances of direct or indirect trauma to the orbitocranial
region accompanied by visual impairment. The initial assessment of a patient
experiencing visual loss post-trauma should commence with a thorough history,
typically obtained from family members, friends, or witnesses to the incident.
However, the examination of a patient suspected of having traumatic optic
neuropathy may be hindered by various patient-related factors, such as concomitant
injuries, level of consciousness, and the patient's ability or willingness to cooperate
during the examination. Following the stabilization of head injury, respiratory, and
cardiovascular concerns, patients should undergo a comprehensive clinical
ophthalmic evaluation..2,5,12
The characteristics of traumatic optic neuropathy include unilateral or bilateral
involvement of the eyes, except in cases of symmetric bilateral TON, presence of
relative afferent pupillary defect, variable decline in visual acuity, impaired color
vision, various visual field defects, and optic disc changes dependent on the location
of the injury along the optic nerve. When the injury occurs anterior to the entry point
of the central retinal vessels, optic disc swelling is observed, while more posterior
injuries, which are more common, typically result in a normal appearing fundus.
Optic atrophy usually becomes apparent around six weeks post-injury. Evaluation of
visual acuity and pupillary reflexes is essential, and funduscopy should be performed
whenever feasible..1-4,9,12
The patient in this case was stable and alert, therefore a complete clinical
ophthalmic evaluation can be obtained. The visual acuity is light perception with
reverse relative afferent pupillary defect on the right eye. Visual fields, color vision
and contras sensitivity as seen in this case, can only be obtained when sufficient
vision is present. It is probably more useful in documenting the return of visual
function following injury in such case.
The pathophysiology of traumatic optic neuropathy (TON) is believed to involve
multiple factors, with the notion of primary and secondary injury being suggested.
Retinal ganglion cells (RGCs), specialized cells within the optic nerve, play a crucial
role in transmitting visual information from the eye to the brain's vision centers.
Primary injury can result in permanent damage to a portion of RGC axons, either
directly or through shearing forces during deceleration, especially within the optic
canal where the nerve is tightly constrained..2,3,4,6,10
The management of suspected optic nerve injury necessitates neuroimaging to
evaluate the injury's extent and identify any accompanying intracranial and facial
injuries, intraorbital fragments, or hematoma. There is no consensus on the optimal
management of patients with traumatic optic neuropathy due to its complex nature,
which often involves both direct and indirect components, as well as primary and
secondary intracellular and extracellular mechanisms of damage..2,3,6,9,11
Evidence indicates that the intracanalicular segment of the optic nerve is
commonly injured, hence nerve decompression, whether through medical or surgical
methods, has been proposed as a treatment. It is theorized that decompression could
mitigate the consequences of optic nerve swelling within the bony canal or
hemorrhagic compression on the nerve and its blood supply, thereby safeguarding
surviving retinal ganglion cells from the initial insults. Current treatment options for
traumatic optic neuropathy include systemic steroids, surgical decompression of the
optic canal, a combination of steroids and surgery, as well as observation or
conservative management..1,3-5,6,9
There was no penetrating wound in this case, therefore traumatic optic neuropathy
is presumed to be the result of an indirect injury. Damage of the optic nerve in this
case can result from both primary and secondary mechanisms. Primary mechanisms
cause permanent injury to the optic nerve axons at the moment of impact. There is
then a degree of optic nerve swelling within the tight confines of the optic canal
secondary to direct mechanical trauma and vascular ischemia. The increasing edema
may lead to compartment syndrome that further impairs the already compromised
blood supply to surviving retinal ganglion cells, setting up toward apoptotic cell
death. The patient in this case was treated by high dose intravenous
methylprednisolone to decrease edematous pressure in the optic canal to reverse
ischemia and axonal conduction block, which can result in irreversible axonal
degeneration.
Steroids have been utilized in the treatment of traumatic optic neuropathy (TON)
since the early 1980s, with the initial pharmacological rationale stemming from
perceived benefits observed in various animal models of central nervous system
injuries. In recent years, evidence has emerged indicating that administering very
high doses of corticosteroids within a few hours of injury can reduce paralysis and the
severity of neurological deficits in patients with acute spinal cord injuries. The effects
of very high dose corticosteroids in experimental models of spinal cord injuries
include a decrease in lipid peroxidation products, improved blood flow in the injured
areas, and enhanced neurophysiological recovery. The results of this clinical trial
have significantly influenced clinical practice, resulting in the increased use of
steroids in the management of traumatic optic neuropathy.2,3,6-9,11,12
The majority of studies on traumatic optic neuropathy (TON) demonstrate a
notable correlation between initial and eventual visual acuities. Patients presenting
with no light perception typically experience limited or no visual improvement.
Additional adverse prognostic indicators include loss of consciousness, absence of
visual recovery beyond 48 hours, and the lack of visual evoke responses. Direct TON
represents a separate category characterized by severe, irreversible visual impairment
with minimal chances of recovery, for which no intervention has been conclusively
proven beneficial.2,6-8
The patient in this case was treated by a course of high dose intravenous
methylprednisolone one gram/day in four divided doses for three days. There was no
adverse affect that occurred during treatment and his response to the treatment was
good with marked visual improvement. The initial visual acuity in this patient was
light perception and the best corrected visual acuity post intravenous
methylprednisolone treatment was 2/60 with snellen measurements. In Traumatic
optic neuropathy, recovery is rarely complete. Subtle visual fields, color vision, and
papillary defect persist despite complete recovery of visual acuity.

IV. Conclusion

Closed globe injuries can manifest in various ways, ranging from eyelid damage to
optic nerve involvement, potentially resulting in traumatic optic neuropathy.
Following optic nerve injury, swelling often occurs, which can exacerbate the
damage. Traumatic optic neuropathy frequently leads to significant visual
impairment, predominantly affecting young males in their thirties. The optimal
management of traumatic optic neuropathy remains a subject of debate; however, the
use of high-dose corticosteroids is currently widely accepted. Steroids are
administered to mitigate the excessive swelling that ensues after optic nerve injury
and to enhance visual recovery. High doses of methylprednisolone may aid in
restoring vision in cases of traumatic optic neuropathy, as demonstrated in the case
being discussed. If vision improves, patients may transition to oral prednisolone with
a tapering dose regimen. In instances of deteriorating vision or lack of improvement
within 48 hours despite intravenous methylprednisolone, surgical decompression may
be considered. Each case of traumatic optic neuropathy requires individual
assessment, and patients should be fully informed about the potential for serious
adverse reactions to steroids, albeit rare.
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