Idiopathic Vitreopapillary Traction: Case Report and Literature Review

Vitreopapillary traction (VPT) syndrome occurs at the vitreopapillary interface. It is characterized by an anteroposterior traction caused by the fibrocellular vitreal membrane pulling at adherent sites on the optic nerve head due to an anomalous posterior vitreous detachment (PVD) causing structural and possible functional impairment [1]. In comparison to vitreomacular traction which has been very extensively studied in numerous publications, less attention has been directed on the clinical effects of persistent attachment of contracting vitreous to the optic nerve head, especially as an isolated phenomenon [2].

We describe a case of idiopathic VPT in a healthy middle-aged male managed with surgical excision of the tractional membrane. We present the following case in accordance with the CARE guidelines. The CARE Checklist has been completed by the authors for this case report, attached as online supplementary material (for all online suppl. material, see https://doi.org/10.1159/000539952).

A 40-year-old male presented to the emergency room with a gradual decrease of vision of the left eye over 3 days duration. There was no history of trauma, pain, prior ocular inflammation, flashes,floaters, or redness. He denies any history of house pets or contact with animals, and his medical and surgical histories were unremarkable. Best-corrected visual acuity was 20/20 in the right and 20/300 in the left eye.

Color vision of the left eye was not applicable, and pupillary assessment showed no anisocoria but with a 0.9 log relative afferent pupillary defect. Anterior segment examination was normal and dilated fundus examination revealed VPT extended beyond the disc margin causing peripapillary retinal and vascular traction mainly inferiorly with secondary preretinal and subretinal hemorrhages. The tractional membrane did not extend to the lens or pull on the anterior segment as is the case in persistent fetal vasculature. The axial length was measured was 23.75 mm in the right eye and 23.70 mm in the left eye. The ophthalmic examination indicated the right eye was essentially normal.

Optical coherence tomography (OCT) revealed a hyperreflective membrane over the optic disc causing tractional thickening with abnormal foveal contour and associated epiretinal membrane. OCT indicated increased thickness of the retinal nerve fiber layer. Goldmann visual field indicated a superior visual field defect worse in temporal quadrant that matched the inferior and inferonasal traction of the optic nerve with split fixation. Fluorescein angiography indicated early hyperfluorescence due to abnormal and dilated vasculature overlaying the tractional membrane (a tiny vascular pattern) with persistent hypoflurescence centrally due to blockage around the lesion secondary to the retinal hemorrhage. There was late hyperfluorescence due to leakage and staining of the lesion (Fig. 1).

Investigations to rule out secondary causes of VPT were performed. Glucose level, complete blood count, coagulation profile, and hemoglobin electrophoresis were all unremarkable. Inflammatory causes including tuberculosis (Quantiferon-TB gold test and Mantoux test) toxoplasmosis, and sarcoidosis (high-resolution computed tomography of the chest and serum angiotensin-converting enzyme), and toxocariasis were all negative.

Given the significant traction and its impact on the visual function, the patient agreed to surgery. The patient underwent chandelier and triamcinolone assisted 23-gauge pars plana vitrectomy with trimming of the tractional membrane and perfluoropropane (C3F8) gas tamponade. A specimen of the membrane was sent for histopathological analysis. The surgery was uneventful with no induced iatrogenic breaks. Histopathology of the membrane indicated small eosinophilic fibroconnective tissue, with spindle-shaped cells (Fig. 2).

Six weeks postoperatively, fundus examination of the left eye revealed relief of traction with settling of the retinal folds and a small subretinal hemorrhage. OCT indicated resolution of traction over the optic disc with a subretinal peripapillary hyporeflective area most likely indicating the site of the hemorrhage Repeat visual fields revealed the same field defects as preoperatively (Fig. 3).VA was maintained at 20/300.

PVD is a dynamic process with the optic nerve as the last site of the detachment, which could explain the strong traction of all forces in the setting of anomalous PVD [1]. In 1942, Sandoz first published a description of the effects of vitreal traction on the papilla with tearing of the glial tissue from the peripapillary region by the shrinking vitreous gel [1‒3]. Katz and Hoyt then detailed the effects of vitreous traction on the optic papilla in 1995 [3]. Their article summarized the features of the condition including, interpapillary hemorrhage, subretinal peripapillary hemorrhage, elevation of the disc, PVD without complete separation from the disc, and preservation of optic nerve function [3].

The pathophysiology of VPT and vitreomacular traction are very similar, both of which develop due to anomalous PVD. VPT can be idiopathic which indicates an abnormal or anomalous PVD which present in elderly patients. More commonly, VPT presents secondary to associated findings that may affected the normal status of the posterior hyaloid such as, cellular proliferation from diseases that potentiate fibrovascular scaffolds for cellular proliferation possibly inducing anomalous PVD [4]. Interestingly, our patient was medically healthy with an unremarkable ocular history. Histopathology of the membrane indicated small fibroconnective tissue, with spindle-shaped cells.

VPT has been proposed as a possible cause of temporary or chronic visual impairment as long-standing optic nerve traction may result in optic atrophy either by impeding the axoplasmic flow or by compromising laminar blood flow through the peripapillary blood vessels [4, 5]. In addition to interference with blood flow as well as axoplasmic flow, VPT may induce multilayered hemorrhage which matches the finding in our patient. Subretinal hemorrhage is the most commonly reported in cases of VPT. The field altitudinal defect in our patient may support the hypothesis that VPT affects the blood flow and induces a picture resembling non-arteritic ischemic optic neuropathy (NAION).

Visual loss and the field loss in VPT have been documented to be reversible after surgery [6]. Multiple publications investigated the structural and functional outcomes after surgical correction [7]. However, conflicting outcomes have been reported with some reports reporting visual improvement and others reporting no improvement [7]. It should be noted that surgical resection of the tractional membrane is preferred when compared to membrane peeling since peeling may induce further tractional forces over the optic disc which can lead to further damage to the optic nerve [7]. Generally, we suggest observation for cases of VPT unless it is associated with significant deterioration of visual function that warrants surgical release to prevent visual compromise. Unfortunately, in our case, the visual field defect and vision remained unchanged after surgery.

Diseases that affect the vitreoretinal interface that include epiretinal membrane and VMT have been investigated extensively in literature. However, the vitreopapillary interface is also an important structure because it is the last and the strongest attachment of the posterior hyaloid. Early detection of VPT may prevent progression to tractional membrane which can induce vision loss. Spectral domain OCT overlying optic nerve head and peripapillary region may allow early detection (Fig. 4), especially in cases that show optic nerve dysfunction with no explainable finding. The pathogenesis of VPT requires further evaluation and investigations.

This retrospective review of patient data did not require ethical approval in accordance with the Hospital and national regulations. The patient provided written informed consent for the publication of the details of their medical case and any accompanying images.

The authors have no conflicts of interest to declare.

None the authors have no funding to declare.

Drs. Abdullah, Alsakran, and Hanbazazh reviewed the medical record, wrote original draft of the case report, and revised intellectual content. Drs. Abdullah, Alsakran, and Hanbazazh critically revised the manuscript and intellectual content.

All data generated or analyzed during this study are included in this article and its online supplementary material files. Further inquiries can be directed to the corresponding author.