FP918 : Clinical Profile and Treatment Outcomes of Traumatic Optic Neuropathy At a Tertiary Eye Care Centre in South India

Dr.Bhushan Uplanchiwar, B15780, Dr. Vinay Kumar.S

_{Bhushan Moreshwar Uplanchiwar DNB}

_{Enquiries to}

_{Bhushan Moreshwar Uplanchiwar}

_{LV Prasad eye institute Hyderabad}

_{email id:chill.04099@gmail.com}

_{Keywords: Indirect Traumatic optic neuropathy, intravenous methyl prednisolone , Road traffic accident}

_{Traumatic optic neuropathy}

_Title

_{Clinical profile and treatment outcomes of traumatic optic neuropathy at a tertiary eye care centre in South India.}

_Aim

_{To evaluate therapeutic outcomes of management in cases of traumatic optic neuropathy}

_{Introduction:}

_{Traumatic optic neuropathy (TON), following blunt or penetrating injuries results in permanent visual loss. While projectiles or other sharp objects injure the optic nerve directly}^1-2_{, the most common form of traumatic optic neuropathy is indirect and, as a result of concussive force to the head, particularly the forehead.  It has been reported 0.5% to 5% of all closed head trauma} ^3-4_.

_{The diagnosis of indirect traumatic optic neuropathy is based on meticulously taken history and clinical examination. However its optimal management is far less well defined. There is endorsement in the literature for corticosteroids (at dosages ranging from 60 mg to 7 g per day), surgical decompression of the optic canal (via intracranial, transethmoidal, endonasal, sub labial, or other approaches), and observation alone}⁵_{. Evidence for the relative benefits of these approaches has mainly been based on small retrospective and anecdotal studies, and therefore a convincing rationale for treatment is lacking. Yet the implications of this disorder are profound, particularly when it is considered that it often affects active young patients. The present retrospective case series was therefore, designed to evaluate the outcomes of different treatment modalities used for treating cases of indirect traumatic optic neuropathy.}

_{Materials and Methods:}

_{A retrospective case series of 35 diagnosed cases of indirect traumatic neuropathy who presented  to a tertiary eye care centre in India in a calendar year.}

_{Inclusion criteria:} 

• _{Indirect traumatic optic neuropathy presenting within 3 months of trauma.}
• _{Minimum follow up of 3 months}

_{Exclusion criteria:}

• _{Direct traumatic optic neuropathy cases due to penetrating injury}
• _{Any injury associated with intracranial injury}
• _{Optic neuritis and other optic nerve head disease}
• _{Late presentation after the injury (>3 months)}
• _{Follow up < 3 months}

_{At baseline visit comprehensive ocular examination was done. The cases identified from the electronic data based on above mentioned criteria, were divided into 5 groups, based on treatment: group I (Oral steroids), group II (Intravenous methylprednisolone (IVMP), group III (IVMP +oral steroids), group IV(IVMP+ orbital decompression) and group (no intervention). Group V included patients who presented within 3 months of injury but did not receive any treatment. The best corrected visual acuity (BCVA) was recorded as Snellen’s fraction and documented in datasheet as LogMar equivalents. The BCVA on presentation and final follow up were compared. Improvement of vision by 2 Snellen’s line was considered as treatment success. Distribution of visual acuity scores among 5 group were compared with chi-square test. In group I oral prednisolone was administered as 1mg/kg in tapering dose for 3-4 weeks. In group II ,  and IV IVMP was administered as 1g/day for 3 days. In Group III IVMP was administered as 1g/day for 3 days followed by oral prednisolone 1mg/kg in tapering dose for 3-4 weeks.}

_Results:

_{26 (74.3%) males and 9 (25.7%) females case charts were reviewed. The mean (SD) age of study group was 29.78 (±13) years. The average duration between the inciting injury and presentation to us was 4.2 days. Mean (SD) visual acuity on presentation was 2.58 (±0.76) on LogMAR scale. Most common cause of TON was road traffic accidents [77%; 95% Confidence interval (CI: 59-88)].}

_{Table 1.}

_{Group wise distribution of male and female:}

	Male (n=26)	Female (n=9)
Group I	6(23%)	4(44%)
Group II	1(3%)	1(12%)
Group III	9(35%)	1(11%)
Group IV	1(4%)	2(22%)
Group V	9(35%)	1(11%)

_{Table : 2}

_{Distribution of mode of injury}

	RTA (n=26)	Accidental fall (n=2)	Alleged assault (n=5)	Unknown (n=2)
Group I	7(70%)	————-	2(20%)	1(10%)
Group II	1(50%)	———–	1(50%)
Group III	9(90%)	1(10%)
Group IV	2(66%)	———	1(33%)
Group V	7(70%)	1(10%)	1(10%)	1(10%)

 _{In the above table road traffic accidentwas the most common mode of injury (77%).}

_{Table: 3}

 _{Table showing Mean Visual Acuity :}

Mean visual acuity	Mean LogMAR value
Group I	1.59
Group II	1.945
Group III	2.55
Group IV	2.34
Group V	2.39

_{Table :4}

Baseline visual Acuity

		Group I	Group II	Group III	Group IV	Group V
No PL		4(19%)	2(9.5%)	6(28.5%)	2(9.5%)	7(33.33%)
PL+				2(40%)	1(20%)	1(20%)
HM		2
CF				2(66%)		1(33%)
1/60
3/60
6/60		3(75%)				1(25%)
6/36		1
6/24
6/18

Table 5

Final visual acuity

		Group I	Group II	Group III	Group IV	Group V
No PL		2(12.5%)	1(6%)	6(37.5%)	1(6%)	6(37.5%)
PL+				1
HM		1(33.3%)			1(33.3%)	1(33.3%)
CF		2(50%)		1(25%)		1(25%)
1/60		1(34%)				2(66%)
3/60					1
6/60		1(33%)		2(66%)
6/36
6/24		2
6/12		1(50%)	1(50%)

 

_{From Table 5 it can be concluded that many patients with indirect traumatic optic neuropathy presented with No PL vision (60%; 95% CI:43-74). Cases that presented with NPL vision had worse prognosis. Group (III and V) had highest number of NPL .  None of the above group showed any gross improvement in visual acuity. Highest BCVA achieved was 6/12 (Group I and II) and Visual acuity improvement was seen in 5 (71%) cases in group I, one (33%) cases in group II, 2(18%) cases in group III, 2 (66%) cases in group IV and 2 (18%) case in group V. The treatment outcomes between the groups were not statistically significant (p 0.1256)} 

_Discussion:

_{The major limitation of this study is that patients presented to us after receiving first-line of intervention, so data on baseline visual acuity was not available. Also there is no data suggesting the time of initiation of therapy. However, the visual outcome in cases of TON was not influenced by the mode of therapeutic interventions.  Specifically, there were no significant differences in final visual acuity, after correction for baseline visual acuity. Likewise, IVMP+ surgery group, there was no clear indication of increased benefit in the patients treated after injury.}

_{The literature does not provide meaningful data for estimating the probability of visual improvement spontaneously, after treatment with corticosteroids, or following decompression of the optic canal. A major difficulty in interpreting many of the reports is how improvement was defined. The majority of reports either do not define visual improvement or consider improvement to be as little as one line of visual acuity. In view of the lack of standardization of visual acuity testing there has been bias in interpretations of results.} 

 _Hughes ^6-7 _{reported an improvement rate of 48% in 56 patients with traumatic optic neuropathy, most of whom were seen during their hospitalization for the injury. Among the 36 patients whose initial visual acuity was NLP, some improvement occurred in 44%, although useful vision  (>3/60) returned in only 17%. Lessell} ⁸ _{reported an improvement rate of 20% in 25 patients with traumatic optic neuropathy; however, the timing of the initial examination was not provided, so the potential for referral bias underestimating the rate cannot be assessed. Because of potential biases and differences in methods among all of the published reports, a comparison across studies or with our study cannot be made with any degree of validity. The one conclusion that can be drawn from the literature is that the prognosis for visual improvement is}

_{worse when there is no light perception following an optic}

_{nerve injury. However, even when visual loss is  severe,}

_{recovery to useful vision without any treatment is possible. Patients can spontaneously recover from TON, and rates of spontaneous improvement have ranged from 20 to 57 percent in published studies.}⁹ _{In the International Optic Nerve Trauma Study, 133 patients with TON were randomized either to corticosteroids or optic canal decompression surgery, or to observation without treatment. The results showed that visual acuity increased by three or more lines in only 32 percent of the surgery group, 52 percent of the steroid group and 57 percent of the untreated group}¹⁰_{. No clear benefit was found for either corticosteroid therapy or optic canal decompression surgery results and the existing literature provide sufficient evidence to conclude that neither corticosteroids nor optic canal surgery should be the standard of care for patients with traumatic optic neuropathy. It is therefore clinically reasonable to decide to treat or not treat on an individual patient basis.}¹¹ 

Conclusion:

The visual outcome in cases of TON was not influenced by the mode of therapeutic interventions in this study.

Drawbacks:

Patient presented to us after receiving first line of intervention so data on baseline visual acuity was not available. Also there is no data suggesting the time of initiation of therapy after the onset of injury.

References:

1. Nazir SA, Westfall CT, Chacko JG, Philips PH, Stack BC Jr. Visual recovery after direct traumatic optic neuropathy. AmJ Otolaryngol 2010;31:19

2. Yu Wai Man, P. and P. G. Griffiths. Cochrane Database Syst Rev 2005;(4):CD005024

3. Carta A, Ferrigno L,Salvo M, Bianchi-Marzoli S, Boschi A, Carta F.Visual prognosis after indirect traumatic neuropathy.J Neurol Neurosurg Psychiatry 2003;74:246-248

4. Indirect traumatic optic neuropathy–two case report. Kovacić M, Gracner T, Gracner B ,Coll Antropol. 2001; 25 Suppl():57-61.

5. Glaser JS. Traumatic optic neuropathy. In: Glaser L, Glaser JS, editors. Neuro-ophthalmology. 3rd ed. Lippincott Williams and Wilkins; 1999. pp. 186–188

6. Cook MV, Levin LA, Joseph MP, et al. Traumatic optic neuropathy: a meta-analysis.Arch Otolaryngol Head Neck Surg1996;122:389–2

7.Hughes B. Indirect injury of the optic nerves and chiasma. Bull  Johns Hopkins Hosp. 1962;111:98–126

8.    Lessell S. Indirect optic nerve trauma. Arch Ophthalmol.             1989;107:382–386

9. Cockerham, K. P. Ophthalmic Care of the Combat Casualty (Falls  Church, Virginia: Office of The Surgeon General, Army, 2003).

10. Levin, L. A. et al. The treatment of traumatic optic neuropathy: the International Optic Nerve Trauma Study. American Academy of Ophthalmology 1999;106(7):1268–1277.

11. Clinical Update: Trauma :Traumatic Optic Neuropathy: Previous Therapies Now Questioned or Shelved:By Barbara Boughton;American Academy of Ophthalmology;The Eye MD _Association