If you don't remember your password, you can reset it by entering your email address and clicking the Reset Password button. You will then receive an email that contains a secure link for resetting your password
If the address matches a valid account an email will be sent to __email__ with instructions for resetting your password
it may precede the development of nonarteritic anterior ischemic optic neuropathy, which can result in permanent vision loss. It is controversial whether DP is actually a mild reversible form of nonarteritic anterior ischemic optic neuropathy.
have been reported. We report a case of DP that was treated with combination panretinal photocoagulation (PRP) laser and intravitreal bevacizumab, which provided sustained and rapid resolution of DP.
A 22-year-old female with poorly controlled diabetes mellitus type I since the age of 2 years presented with blurry vision and transient visual obscurations in both eyes. Her hemoglobin A1C was 12.2%, and she was recently an inpatient for diabetic ketoacidosis. She denied any headaches, her baseline weight was around 130 pounds, and she had no other systemic diseases. Her vision at presentation was 20/100 OD and 20/25 OS. Intraocular pressure was normal OU. Slit-lamp examination was unremarkable OU. Dilated examination revealed profound disc edema OD and mild disc edema OS (Fig. 1A, 1B). The patient had severe nonproliferative diabetic retinopathy (NPDR) OU. There was no clinically significant diabetic macular edema OU. Fluorescein angiography revealed profound hyperfluorescence at the optic nerve OD > OS, with multiple patchy areas of intraretinal microvascular abnormalities and peripheral capillary nonperfusion (Fig. 2). Optical coherence tomography (OCT) of the optic nerve quantified the degree of retinal nerve fibre layer thickening (OD 359 μm, OS 157 μm). OCT of the macula showed a sliver of subfoveal fluid and marked fluid emanating from the nerve to within a disc diameter of the fovea centre OD. There was optic nerve edema OS, but no subfoveal fluid or cystoid macular edema.
The patient was treated with combined intravitreal bevacizumab and staged PRP OD. At 1-month follow-up, her vision improved to 20/25 OD with complete resolution of her disc edema and subretinal fluid between the fovea and optic nerve. She received another injection of bevacizumab and fill-in PRP OD. At 2-month follow-up, there was no recurrence of her disc edema and the telangiectatic leaking papillary vessels were extinguished (Fig. 1C, 1D). Meanwhile, the left eye continued to have mild disc edema and severe NPDR. The patient elected for observation at that time. At 6-month follow-up, the patient’s vision remained excellent with no signs of recurrent DP or proliferative disease (Fig. 1E, 1F). The OCT of the optic nerve showed an average retinal nerve fibre layer thickness of OD 98 μm and OS 133 μm.
The patient’s DP regressed very rapidly with combined treatment using scatter PRP and intravitreal bevacizumab. Although visual prognosis without treatment is often favourable in these cases, it generally takes a prolonged period to improve.
PRP has never been described as a treatment option for DP, and it may also have utility in preventing the complications arising from severe NPDR such as vitreous hemorrhage, subsequent vitrectomy, and visual impairment.
The mechanism of action of bevacizumab in DP is not well understood; however, the accelerated response to bevacizumab combined with scattered laser suggests that vascular endothelial growth factors play an important role in the pathogenesis of this condition. Prior reports of accelerating improvement of DP with intravitreal and periocular corticosteroids suggest that an inflammatory component could also be involved in the pathogenesis of this disorder.
The patient’s untreated left eye serves as a surrogate control for persistent papillopathy and high-risk retinopathy; however, additional studies are needed to determine the exact efficacy and safety of this combined treatment.
The authors thank Dr. Randy H. Kardon for his review of this manuscript.
Diabetic papillopathy in type II diabetic patients.