| As is known diabetes mellitus and arterial sclerosis could easily lead to ischemia optic neuropathy. However, with the research of diabetic retinopathy progressed, clinical use of Optical Coherence Tomography(OCT), re-recognition of the vitro-retinal diseases and progress of vitrectomy technology, it has been proved that a kind of tractional diabetic neuropathy caused by optic traction could be found in DR patients. This may be an important reason leading to damage of the visual function of DR patients. Research of this kind of disease just shows up nowadays abroad, and none has been reported internal. Since many ophthalmologists don't know it amply, our trial investigates the tractional effect of incomplete vitreous detachment and fibrovascular membrane before the optic area on optic in two parts respectively. And try to conclude the mechanism of tractional diabetic optic neuropathy.Part I Incomplete vitreous detachment and tractional diabetic optic neuropathyPurpose: Aim to analyze the relationship between incomplete vitreous detachment and tractional diabetic optic neuropathy. To evaluate the pathogenesis mechanisms of tractional diabetic optic neuropathy.Methods: 11 patients (17 eyes) with papilledema other than optic edema caused by optic ischemia were given BCVA, fundus examination, FFA, OCT, VEP, visual field. No interventions was given, after 1-year's follow up, clinical examination results was recorded. 3M, 6M and 9M after baseline, BCVA, Fundus examination were given, and OCT was given to observe the traction between posterior vitreous cortex and disc。1 year later,the 6 examinations mentioned above were given again.Results: 1 BCVABCVA at first visit was 0.45±0.32. The BCVA of return visit at 3M,6M,9M and 1Y was 0.48±0.66, 0.41±0.33, 0.44±0.42, 0.44±0.73. There was no difference between the BCVA at different follow-up point and baseline.2 leaking area of optic edemaThe leaking area of optic edema at baseline was (19.85±15.06)mm2 , 1 year later it was (20.02±13.77)mm2 , and there was no difference between them. During 1-year follow-up, there are 2 eys (11.76%) developed complete vitreous detachment with a reduced leaking area of(5.27±3.77)mm2 .3 OCTThere are 14 eyes(82.35%) represented high-reflective band traction upon optic of incomplete vitreous detachment, and there are many traction adhesion between the posterior vitreous cortex and optic or retinal elsewhere. 1 year later, 2 eyes developed complete vitreous detachment, the optic traction disappeared, and the optic edema disappeared while 15 eyes still represent optic traction.The optic elevation at first visit was (314.36±20.24)μm. The optic elevation of return visit at 3M,6M,9M and 1Y was (323.42±19.92)μm, (343.23±30.98)μm, (378.56±29.48)μm, (388.12±27.27)μm. There was no difference between every visit point and baseline. 2 eyes which developed complete vitreous detachment with an elevation of (126.48±79.62)μm, and the optic edema significantly lightened.4 VEP (the P100 latency)15/17 eyes(88.23%) showed a longer P100 latency at baseline, while 2 eyes(11.76%) with a normal P100 latency. P100 latency was (118.87±12.54)ms, 1year later it was (109.12±3.99)ms, between them there was no difference.1 year later 2 eyes which developed complete vitreous detachment with a reduced P100 latency (108.27±16.55)ms.5 The mean sensitivity and the mean defect of 300Visual fieldAt baseline, there were 11 eyes(64.70%) with a larger physiological blind spot, and 3 eyes(17.64%)with a centre scotoma, 1 eye with a arciform visual field defect.The mean sensitivity of 300Visual field at baseline was (18.50±4.77) dB, 1year later it changed to (19.45±4.58) dB, there was no difference between the two points. 1 year later 2 eyes which developed complete vitreous detachment with an improved mean sensitivity of 300Visual field (22.86±4.66)dB.At baseline the mean defect of 300Visual field wa(s3.31±0.45)dB, 1 year later it had changed to(3.71±1.56)dB, there was no difference between the two time points. 1 year later 2 eyes which developed complete vitreous detachment with an reduced mean defect of 300Visual field(22.86±4.66)dB.Conclusions:1 Vitreopapillary traction caused by incomplete vitreous detachment plays an important part in the pathogenesis formation of papilledema with tractional diabetic optic neuropathy.2 Once the papilledema caused by vitreopapillary traction disappeared, the visual function can partially recover in DR patients.Part II Traction of fibrovascular membrane on disc and tractional diabetic optic neuropathyPurpose: Aim to investigate the relation between fibrovascular membrane on disc and tractional diabetic optic neuropathy, and the mechanisms of tractional diabetic optic neuropathy. To evaluate the effect of vitrectomy and membrane peeling to tractional diabetic optic neuropathy.Methods: 8 patients of proliferative diabetic retinopathy with optic fibrovascular membrane without or with mild maculapothy which couldn't explain the severe decreased vision were given BCVA, fundus examination, fundus photography, FFA, OCT, VEP, and visual field examinations. Then they accepted vitrectomy combined with membrane peeling. After the operation 6 examination mentioned above were given. Results:1 BCVA1M after operation BCVA were improved from 0.06士0.04 to 0.15士0.08. 3M after operation BCVA were improved to 0.34士0.17. Compare BCVA before and after operation, BCVA improved after operation, and the difference is meaningful(P<0.05). Compare BCVA 1m and 3m after operation, the difference is meaningful(P<0.01).2 OCTThere are 6 eyes with an optic elevation>300μm before operation, and 5 eyes with a elevation between (200-300)μm. The average elevation is (300.64士48.90)μm. 1m after operation there are 4 eyes with an optic elevation>300μm. 5 eyes with an elevation between (200-300)μm and 1 eye with a elevation <200μm. The average elevation is (260.35士39.11)μm. 3M after operation there are 9 eyes with an optic elevation <200μm, and 2 eyes with an elevation between (200-300)μm. The average elevation is (164.36士30.81)μm. Compare the elevation 1M after operation and before, the difference is significant. Compare the elevation 3M after operation and before, the difference is significant. (P<0.05)3 Fluorescence leaking area of optic edemaBefore the operation, the leaking area of optic edema is (17.46士10.23)mm2 ,3M after operation the leaking area reduced to (9.33士8.95) mm2 . Compare the leaking area before and 3M after operation, the difference is significantly meaningful(P<0.01).4 VEP( the P1 latency and amplitude )Before the operation the average P1 latency was (200.36士40.26)ms, and 3M after the operation it had reduced to (171.27士34.40)ms. Compare the P1 latency before and 3M after the operation, the difference is significantly meaningful (P=0.018).Before the operation the average P1 amplitude is (4.87士3.77)μνand 3M after the operation, it has increased to (7.23士3.30)μν. Compare the amplitude of P1before and 3M after the operation, the difference is significantly meaningful(P=0.013). 5 Visual fieldBefore the operation the mean sensitivity of 300Visual field was(16.36士0.24)dB, and 3M after the operation it had improved to (21.14士2.55)dB. Compare the mean sensitivity of 300Visual field before and 3M after the operation, the difference is significantly meaningful(p<0.01).Before the operation the mean defect is (22.55士2.86)dB, and 3M after the operation it had decreased to (12.85士2.13)dB. Compare the mean defect before and 3M after the operation, the difference is significantly meaningful(p<0.01).Conclusions1 The fibrovascular membrane upon the optic can lead to Vitreopapillary traction and tractional diabetic optic neuropathy which can result in severe vision damage in PDR patients.2 Vitrctomy can release the vitreopapillary traction of fibrovascular membrane and it is an effective measure to tractional diabetic neuropathy which can lead to recovery of visual function.
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