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 Table of Contents    
LETTER TO THE EDITOR
Year : 2015  |  Volume : 8  |  Issue : 1  |  Page : 75-76  

Role of total dose and hyperfractionation in reducing risk of radiation-induced optic neuropathy


1 Department of Opthalmology, Government Medical College, Nagpur, Maharashtra, India
2 Department of Forensic Medicine, Government Medical College, Nagpur, Maharashtra, India

Date of Web Publication23-Jan-2015

Correspondence Address:
Nilesh K Tumram
Department of Forensic Medicine, Government Medical College, Nagpur - 440 003, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-620X.149901

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How to cite this article:
Kumre D, Jeswani V, Benurwar S, Tumram NK. Role of total dose and hyperfractionation in reducing risk of radiation-induced optic neuropathy. Oman J Ophthalmol 2015;8:75-6

How to cite this URL:
Kumre D, Jeswani V, Benurwar S, Tumram NK. Role of total dose and hyperfractionation in reducing risk of radiation-induced optic neuropathy. Oman J Ophthalmol [serial online] 2015 [cited 2019 Nov 19];8:75-6. Available from: http://www.ojoonline.org/text.asp?2015/8/1/75/149901

Sir,

Radiation-induced optic neuropathy (RION) is one of the most disabling late complications that may occur in patients treated with radiotherapy (RT) for head-and-neck cancer. [1] It is caused by ischemia of the optic nerve. Ischemic optic neuropathy is classified as anterior or posterior depending on the location of the injury. It appeared that  altered fractionation might be associated with a lower risk of RION. [1] Fractionation by conventional means is of once daily dose while the hyperfractionation consist of two or more than twice daily dose of RT.

Between April 2012 and March 2013, 98 patients (58 M and 40 F) with tumors of the nasopharynx, paranasal sinuses, and nasal cavity were treated with curative intent at our institution. Patients were examined around 1 year after RT completion. Patients were excluded if the optic nerves and optic chiasm were outside the treatment fields or near the field edge, received prior RT to the same site, had any ocular or systemic disease affecting optic disc, are taking chemotherapy, had visual problems before RT that could have contributed to vision loss. 33.67% patients had nasopharyngeal tumors, 33.67% had paranasal sinus neoplasms, 22.44% had nasal cavity lesions, and hard palate malignancies. The histologic distribution is depicted in [Table 1].
Table 1: Tumor histologic types

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Ophthalmologic evaluation of these patients was done by Ishihara chart, indirect opthalmoscopy, fundus fluorescein angiography, Optical coherence tomography and automated perimetry,   irrespective of whether visual problems developed. The primary endpoint of this study was the  ophthalmologic diagnosis of RION. This was done by examining (i) hard exudates, cotton wool spots and superficial hemorrhages around the optic disc; (ii) disc edema; (iii) history of head and neck RT received. Exclusion criteria: Patients were excluded if the optic nerves and optic chiasm were outside the treatment fields or near the field edge (the latter making accurate dose calculations difficult), if they had received prior RT to the same site, if they had any ocular or systemic disease affecting optic disc, if they are taking chemotherapy, if they had visual problems before RT that could have contributed to vision loss.

Patients who had no evidence of RION but who experienced loss of vision from other causes (e.g. dry eye syndrome) were excluded. Patients who lost vision in one eye but not the other were retained, and the functional eye was evaluated.

Out of the 98 patients, nine patients (9%) developed RION in 14 eyes. Out of the nine patients, three patients developed anterior optic neuropathy and six patients posterior optic neuropathy. RION was unilateral in five patients (anterior in two patients and posterior in three patients) and was bilateral in four patients (anterior in one patient and posterior in three patients). The risk of RION according to the total dose, dose/fraction, and the once-versus twice a day fractionation [Table 2].
Table 2: Risk of optic neuropathy versus dose per fraction and fractionation schedule

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Of 58 patients treated with once-daily RT, 8 (13.7%) developed RION compared with 1 (2.5%) of 40 patients treated with twice-daily RT. Of the patients treated with once a day RT, the risk of RION increased with the dose per fraction >1.7 Gy. [Table 3] Data pertaining to the risk of developing RION after RT for head-and-neck tumors are relatively limited. [2] The risk of RION increased with age, particularly for those 50 years. [1]
Table 3: Relationship of age and RION

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Sublethal damage repair has been shown to take place in tissues that are mitotic, but whether this occurs to a significant degree in a 6-h interfraction interval in differentiated, fixed, postmitotic tissue, such as neural tissue, remains controversial. [3] As, the initial target of the radiation damage may be vascular endothelial tissue, hyperfractionation may reduce the risk of this injury and thus the likelihood of developing RION. [4],[5] Our data showed a decrease in the occurrence of RION after hyperfractionation compared with once-daily RT.

 
   References Top

1.
Parsons JT, Bova FJ, Fitzgerald CR, Mendenhall WM, Million RR. Radiation optic neuropathy after megavoltage external-beam irradiation: Analysis of time-dose factors. Int J Radiat Oncol Biol Phys 1994;30:755-63.  Back to cited text no. 1
    
2.
Brown GC, Shields JA, Sanborn G, Augsburger JJ, Savino PJ, Schatz NJ. Radiation optic neuropathy. Ophthalmology 1982;89:1489-93.  Back to cited text no. 2
    
3.
Chan RC, Shukovsky LJ. Effects of irradiation on the eye. Radiology 1976;120:673-5.  Back to cited text no. 3
    
4.
Van Balen AT, Pigeaud-Klessens ML. Radiation-retino and opticopathy. Doc Ophthalmol 1988;68:239-45.  Back to cited text no. 4
    
5.
Parsons JT, Bova FJ, Fitzgerald CR, Mendenhall WM, Million RR. Tolerance of the visual apparatus to conventional therapeutic irradiation. In: Gutin PH, Leibel SA, Sheline GE, editors. Radiation injury to the nervous system. New York: Raven Press; 1991. p. 283-302.  Back to cited text no. 5
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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