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 Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 5  |  Issue : 2  |  Page : 32-34

Role of retrobulbar dexamethasone in the treatment of optic neuritis


Nayan Jyoti Eye Care Centre, Kolkata, West Bengal, India

Date of Web Publication19-Feb-2019

Correspondence Address:
Dr. Sourav Kumar Bose
Nayan Jyoti Eye Care Centre, 9, Jessore Road, Kazipara, Kolkata - 700 028, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/erj.erj_10_18

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  Abstract 


Optic neuritis is a disease entity characterized by, as the name clearly suggests, inflammation of the optic nerve. Over many years, the treatment of optic neuritis has been the use of steroids. The Optic Neuritis Treatment Trial laid the foundation stone for calibrating the use of steroids. However, all modalities have their own adverse effects, in terms of cost, patient compliance, adverse effects, etc. The purpose of this article is to evaluate the role of retrobulbar dexamethasone in the treatment of optic neuritis. After proper patient preparation, a neuritic cocktail of dexamethasone and lignocaine, in pretitrated amounts, is injected in the retrobulbar space. This was administered 3 times at an interval of 48 h, followed by oral prednisolone and supplemented with oral Vitamin B complex. Of 14 patients, 8 (57.1%) patients gained to a best-corrected visual acuity (BCVA) of 6/12 or more, 4 (28.5%) patients had BCVA between 6/24 and 6/18, and 2 (14.2%) patients had BCVA of 6/60. Hence, we conclude that such affordable drug combination can provide a cost-effective measure to treat optic neuritis.

Keywords: Dexamethasone, optic neuritis, retrobulbar injection


How to cite this article:
Bose SK, Bose G. Role of retrobulbar dexamethasone in the treatment of optic neuritis. Egypt Retina J 2018;5:32-4

How to cite this URL:
Bose SK, Bose G. Role of retrobulbar dexamethasone in the treatment of optic neuritis. Egypt Retina J [serial online] 2018 [cited 2019 Sep 18];5:32-4. Available from: http://www.egyptretinaj.com/text.asp?2018/5/2/32/252537




  Introduction Top


Optic neuritis is a disease entity characterized by, as the name clearly suggests, inflammation of the optic nerve. It usually affects young adults, especially females aged between 18 and 45 years of age. Although it has been reported from almost all parts of the world, regions with the highest incidence include Northern Europe, Southern Australia, and middle part of North America.[1] Indian studies have shown that multiple sclerosis (MS) constitutes 0.32%–1.58% of neurology admissions in hospitals,[2] and a prevalence of approximately 1.33/100,000 was reported by Singhal et al. in the mid-80s from the west coast of India.

Typical optic neuritis in adults usually presents as acute uniocular visual loss progressing over several hours to days. It may often be associated with ocular pain that worsens on eye movement. The visual acuity may range from 6/6 to perception of light (PL). Bilateral optic neuritis may also occur, either simultaneously or sequentially,[3] which would also be an unusual feature in typical optic neuritis.[4] Whatever may be the presentation, it has a profound effect on the lifestyle of the patient concerned, and hence, a fast and effective treatment must be sought.


  Procedure Top


The study was conducted on 14 patients, visiting the outdoor of the institute. The presence of MS was ruled out after neurologist consultation. After proper consent, the patients were selected for the treatment. The procedure was performed in the minor operation theater. Lignocaine sensitivity skin test was performed in all patients to exclude those showing anaphylactic reaction. The other exclusion criteria included presence of diabetes, diagnosed demyelinating disease, age <16 years, pregnant women, breastfeeding women, known allergy to any of the drugs used or their components, and coexisting retinal/vitreous disorders.

The “neuritic cocktail” was prepared by mixing 1.5 ml of dexamethasone sodium phosphate (4 mg/ml) and 0.5 ml of lignocaine hydrochloride (20 mg/ml) in a 2 ml disposable syringe, attached to an Atkinson 25-gauge retrobulbar needle. The periocular area around the affected eye was swabbed with 10% povidone-iodine, followed by ethyl alcohol. One drop of 0.5% proparacaine hydrochloride was instilled in the conjunctival sac, followed by two drops of diluted (1:2) 5% povidone-iodine, left in situ for 3 min, and then washed off.

The patient is instructed to lie supine, open his/her eyes, and look upward toward the surgeon, sitting at the head end. The lower fornix is hence better exposed. The needle is inserted at the junction of the lateral one-third and medial two-thirds of the inferior orbital margin by puncturing the forniceal conjunctiva, beveled end facing the globe. As the “give away” sensation is felt and the hub of the needle reaches the orbital margin, confirming that the tip is at the retrobulbar space, the drug is pushed out gradually. After the syringe is empty, it is gently pulled out. When properly administered, the procedure is completely painless and very comfortable. A drop of 0.5% moxifloxacin is instilled in the eye, and the patient is let go.

The cocktail was repeated at an interval of 48 h for 3 such. This was followed by a coarse of oral prednisolone (after breakfast) 20 mg/day for 1 week and then 10 mg/day for 1 week along with oral pantoprazole 40 mg a day before breakfast. During the entire duration of treatment, the patient was also kept on a supplementation of Vitamin B1 + B6 + B12 (100 mg + 100 mg + 5 mg, respectively), which also continued for 1 week more (after stopping oral prednisolone).

All patients were kept in follow-up at 1, 2, and 6 months.

There was a gain in visual acuity of the patient. Of 14 patients, 8 (57.1%) patients gained to a best corrected visual acuity (BCVA) of 6/12 or more, 4 (28.5%) patients had BCVA between 6/24 and 6/18, and 2 (14.2%) patients had BCVA of 6/60. There was no incidence of relapse at the stipulated time.


  Conclusion Top


Over many years, the treatment of optic neuritis has been the use of steroids. The Optic Neuritis Treatment Trial (ONTT) laid the foundation stone for calibrating the use of steroids.[5] Studies with higher doses of oral corticosteroids (methylprednisolone) versus placebo have been conducted, but no statistically significant benefit could be seen on a long-term basis or in the relapse rate.[6] An observational study evaluated the efficacy and safety profile of intravenous dexamethasone showed that the intravenous pulse dexamethasone led to rapid recovery of vision in acute optic neuritis, without any serious side effects.[7] Intravenous dexamethasone was found to be as effective as high-dose intravenous methylprednisolone therapy, as recommended by the ONTT study.[8] Immunomodulators have also been of proven use in the management of optic neuritis, both myelinating and demyelinating.[9],[10],[11]

Dexamethasone comes at a price of about a sixth of methylprednisolone and even lesser than immunomodulators. Intravenous pulse methylprednisolone and immunomodulators have serious well known adverse effects.[12],[13] Retrobulbar injection of the same ensures avoidance of its side effects, when administered systemically.[14],[15] The procedure takes about 2 min, and the patient can be sent home right after injection. The propensity of intraocular pressure rise with dexamethasone is very less.[16] The only risk loophole of this procedure is the practice of retrobulbar drug injection, which, however, can be avoided by proper administration technique.[17]

The “neuritic cocktail” of retrobulbar dexamethasone with lignocaine followed by oral steroid and Vitamin B supplementation is a fast, effective, and reliable way to restore vision in a patient with demyelinating optic neuritis.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Pugliatti M, Sotgiu S, Rosati G. The worldwide prevalence of multiple sclerosis. Clin Neurol Neurosurg 2002;104:182-91.  Back to cited text no. 1
    
2.
Chopra JS, Radhakrishnan K, Sawhney BB, Pal SR, Banerjee AK. Multiple sclerosis in North-West India. Acta Neurol Scand 1980;62:312-21.  Back to cited text no. 2
    
3.
Pirko I, Blauwet LA, Lesnick TG, Weinshenker BG. The natural history of recurrent optic neuritis. Arch Neurol 2004;61:1401-5.  Back to cited text no. 3
    
4.
Hickman SJ, Dalton CM, Miller DH, Plant GT. Management of acute optic neuritis. Lancet 2002;360:1953-62.  Back to cited text no. 4
    
5.
Cleary PA, Beck RW, Anderson MM Jr., Kenny DJ, Backlund JY, Gilbert PR, et al. Design, methods, and conduct of the optic neuritis treatment trial. Control Clin Trials 1993;14:123-42.  Back to cited text no. 5
    
6.
Sellebjerg F, Nielsen HS, Frederiksen JL, Olesen J. A randomized, controlled trial of oral high-dose methylprednisolone in acute optic neuritis. Neurology 1999;52:1479-84.  Back to cited text no. 6
    
7.
Sethi HS, Menon V, Sharma P, Khokhar S, Tandon R. Visual outcome after intravenous dexamethasone therapy for idiopathic optic neuritis in an Indian population: A clinical case series. Indian J Ophthalmol 2006;54:177-83.  Back to cited text no. 7
[PUBMED]  [Full text]  
8.
Menon V, Mehrotra A, Saxena R, Jaffery NF. Comparative evaluation of megadose methylprednisolone with dexamethasone for treatment of primary typical optic neuritis. Indian J Ophthalmol 2007;55:355-9.  Back to cited text no. 8
[PUBMED]  [Full text]  
9.
Jacobs LD, Beck RW, Simon JH, Kinkel RP, Brownscheidle CM, Murray TJ, et al. Intramuscular interferon beta-1a therapy initiated during a first demyelinating event in multiple sclerosis. CHAMPS Study Group. N Engl J Med 2000;343:898-904.  Back to cited text no. 9
    
10.
PRISMS Study Group and the University of British Columbia MS/MRI Analysis Group. PRISMS-4: Long-term efficacy of interferon-beta-1a in relapsing MS. Neurology 2001;56:1628-36.  Back to cited text no. 10
    
11.
Kappos L, Polman CH, Freedman MS, Edan G, Hartung HP, Miller DH, et al. Treatment with interferon beta-1b delays conversion to clinically definite and mcDonald MS in patients with clinically isolated syndromes. Neurology 2006;67:1242-9.  Back to cited text no. 11
    
12.
O'Connor P, Kinkel RP, Kremenchutzky M. Efficacy of intramuscular interferon beta-1a in patients with clinically isolated syndrome: Analysis of subgroups based on new risk criteria. Mult Scler 2009;15:728-34.  Back to cited text no. 12
    
13.
Jongen PJ, Stavrakaki I, Voet B, Hoogervorst E, van Munster E, Linssen WH, et al. Patient-reported adverse effects of high-dose intravenous methylprednisolone treatment: A prospective web-based multi-center study in multiple sclerosis patients with a relapse. J Neurol 2016;263:1641-51.  Back to cited text no. 13
    
14.
Vardy J, Chiew KS, Galica J, Pond GR, Tannock IF. Side effects associated with the use of dexamethasone for prophylaxis of delayed emesis after moderately emetogenic chemotherapy. Br J Cancer 2006;94:1011-5.  Back to cited text no. 14
    
15.
Halvorsen P, Raeder J, White PF, Almdahl SM, Nordstrand K, Saatvedt K, et al. The effect of dexamethasone on side effects after coronary revascularization procedures. Anesth Analg 2003;96:1578-83.  Back to cited text no. 15
    
16.
Srinivasan R, Sharma U, George R, Raman R, Sharma T; Sankara Nethralaya Vitreoretinal Study Group (SNVR Study Group), et al. Intraocular pressure changes after dexamethasone implant in patients with glaucoma and steroid responders. Retina. 2017; doi: 10.1097/IAE.0000000000001924. [Epub ahead of print].  Back to cited text no. 16
    
17.
Fahmi A, Bowman R. Administering an eye anaesthetic: Principles, techniques, and complications. Community Eye Health 2008;21:14-7.  Back to cited text no. 17
    




 

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