Resolution of diabetic papillopathy after a single intravitreal injection of ranibizumab

Authors

  • Anne Willerslev,

    1. Department of Ophthalmology, Glostrup Hospital, Glostrup, Denmark
    2. Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark
    Search for more papers by this author
  • Inger Christine Munch,

    1. Department of Ophthalmology, Glostrup Hospital, Glostrup, Denmark
    2. Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark
    Search for more papers by this author
  • Michael Larsen

    1. Department of Ophthalmology, Glostrup Hospital, Glostrup, Denmark
    2. Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark
    Search for more papers by this author
    • ML has served as a consultant for Novartis on behalf of the Glostrup Hospital.


Anne Willerslev
Department of Ophthalmology
Glostrup Hospital
2600 Glostrup
Denmark
Tel: + 45 3863 4834
Fax: + 45 3863 4834
Email: oejenforsk@glo.regionh.dk

Editor,

Diabetic papillopathy is defined as oedema of the optic disc of no detectable aetiology other than diabetes. Here, we describe a case of diabetic papillopathy that resolved shortly after the administration of an intravitreal inhibitor of vascular endothelial growth factor.

A 28-year-old woman with type 1 diabetes since the age of 5 years was referred with proliferative retinopathy. She was treated in both eyes with peripheral retinal laser photocoagulation and a single session of photocoagulation for diabetic macular oedema. Meanwhile, insulin treatment was intensified, and the HbA1c-level went from 10.8%, the value of the most recent blood sample before metabolic control was intensified, to 7.7%. After 2 months, retrohyaloid haemorrhage led to vitrectomy in both eyes with silicone oil tamponade in the left eye, where traction retinal detachment was imminent. The optic disc in the right eye had been normal 2 weeks after vitrectomy, but another 2 weeks later, the patient was found to have optic disc oedema and disc-centred intraretinal cystoid oedema in both eyes, extending up to the fovea but not involving its centre (Fig. 1). Best-corrected visual acuity (BCVA) was 0.3 in the right eye and 0.05 in the left eye.

Figure 1.

 Fluorescein angiogram (11 min, top) and transfoveal optical coherence tomogram (second from top) from the right eye of a 28-year-old woman with type 1 diabetes who presented with diabetic papillopathy and best-corrected visual acuity 0.3 in her right eye early after having experienced a pronounced and lasting reduction in glycaemia. Gradual resolution of the optic nerve head oedema and peripapillary retinal oedema was detectable at 2 weeks (third from top) and 7 months (bottom) after a single intravitreal injection of ranibizumab 0.5 mg. Final best-corrected visual acuity was 0.9.

The patient did not have headache, nausea, tinnitus or signs of cranial nerve compression. Blood pressure was normal, and computed X-ray tomograms of the brain and orbits were unremarkable, for which reason we considered idiopathic intracranial hypertension, intracranial tumour and inflammatory papilloedema unlikely and chose diabetic papillopathy as our action diagnosis.

Because vascular leakage appeared to contribute to the disc oedema, the patient was given an intravitreal injection of ranibizumab 0.5 mg (Lucentis; Novartis, Basel, Switzerland) in the right eye after informed consent to the off-label treatment had been obtained. This was followed within 2 weeks by marked reduction in the optic disc oedema (Fig. 1) and BCVA improvement to 0.8. Ranibizumab injection in the left eye was not considered because of the silicone tamponade. Six months after the injection of ranibizumab, BCVA was 0.9 in the right eye, where disc oedema was absent and the cup-disc ratio was 0.2 (Fig. 1), while BCVA was 0.3 in the left eye, where the silicone oil had been removed and foveomacular traction was present. Severe fibrosis at the optic disc made it impossible to estimate the amount of disc oedema in the left eye.

In the present case, diabetic papillopathy had largely resolved 2 weeks after intravitreal ranibizumab injection, while BCVA had improved from 0.3 to 0.8. The patient had experienced a drastic reduction in glycaemia prior to the development of diabetic papillopathy and she had small discs, both of which are risk factors for diabetic papillopathy (Ostri et al. 2010). The spontaneous course of diabetic papillopathy tends to be more protracted with regression of the disc oedema occurring over months and visual recovery often being incomplete (Ostri et al. 2010). Diabetic papillopathy had not reappeared in our patient at the one-year follow-up, which is twelve times longer than the effective duration of VEGF-inhibition after a single ranibizumab injection. This suggests that ranibizumab may have been of benefit in relieving diabetic papillopathy in our patient. The presumed mode of action of ranibizumab would involve inhibition of vascular endothelial growth factor, which led to a reduction in vascular exudation and extracellular fluid accumulation, which again led to reduced venous congestion, which led to improved perfusion and reduced retinal nerve fibre swelling and so on. The long-lasting effect of a single injection of ranibizumab suggests that habituation of the retina to improved metabolic control also may have assisted in stabilizing her condition (Holfort et al. 2011). A comparable course of recovery of diabetic papillopathy after a single intravitreal injection of bevacizumab, another inhibitor of vascular endothelial growth factor, has previously been described, but without imaging studies (Ornek & Ogurel 2010). Our observations suggest that intravitreal inhibition of vascular endothelial growth factor may be of therapeutic benefit in eyes with diabetic papillopathy.

Ancillary