Spontaneous regression and quiescence of choroidal neovascularization secondary to traumatic choroidal rupture depicted on OCT angiography

Introduction

Choroidal rupture is defined as a tear or break within the Bruch's membrane, retinal pigment epithelium and choroid that is usually a result of either blunt non-penetrating closed-globe ocular injury or indirect trauma. ¹ Bruch's membrane lacks the tensile strength and elasticity characteristic of the sclera and retina respectively. Hence, during blunt trauma, mechanical compression and sudden hyperextension leads to tears in the Bruch's membrane and damage to choroidal vessels causing hemorrhages beneath the retinal pigment epithelium and subretinal space. ¹ Vision may be compromised either due to formation of a secondary choroidal neovascular membrane, hemorrhagic and/or serous macular detachment or optic nerve pallor.^1,2

Choroidal neovascularization is a well-known complication of traumatic choroidal rupture.^1,2 Typically, choroidal neovascularization secondary to traumatic choroidal rupture is treated with anti-vascular endothelial growth factor (anti-VEGF) therapy in the form of Bevacizumab.^3–5 Usually, 1–3 injections of Bevacizumab may be required to cause inactivation and regression of choroidal neovascularization. ⁵

Since the introduction of optical coherence tomography (OCT) angiography, a non-invasive evaluation of retinal and choroidal microvasculature in different posterior segment conditions, monitoring of choroidal neovascular complexes and assessment of the ischemic changes in the retina has become possible. ⁶ Isolated case reports and case series have described the detection and evolution of choroidal neovascularization secondary to traumatic choroidal rupture treated with anti-VEGF therapy using OCT angiography.^3–5,7,8 Using this non-invasive technology, the present case describes early detection of choroidal neovascular membrane secondary to traumatic choroidal rupture and its spontaneous regression and quiescence without treatment.

Case description

A previously healthy 19 year old female presented to the retina clinic at Louisiana State University Health Care Network, New Orleans, LA in March 2021 with decreased vision in her left eye following a blunt non-penetrating closed globe injury two weeks prior. A complete ophthalmological examination including a dilated fundus examination was performed. A verbal consent to publish details of the clinical presentation and images was obtained from the patient.

On exam, her best corrected visual acuity was counting fingers at two feet in the left eye and 20/20 in the right eye. Intraocular pressure was 17 in the left 18 in the right eye. Slit lamp biomicroscopy of the left eye showed trace subconjunctival hemorrhage. Rest of the anterior segment examination of the left eye was normal. Dilated fundus examination of the left eye was significant for a fovea involving vertical choroidal rupture and overlying subretinal hemorrhage. Anterior segment and dilated fundus examination of the right eye were normal.

She underwent color fundus photography (Optos®, California, USA) that showed subretinal hemorrhage overlying the vertical choroidal rupture through the foveal center. Fundus autofluorescence (Spectralis HRA imaging system; Heidelberg Engineering, Germany) was consistent with fovea involving choroidal rupture and juxtafoveal areas of retinal pigment epithelial degeneration. Structural OCT (Spectralis OCT2 Module; Heidelberg Engineering, Heidelberg, Germany) revealed a break in the retinal pigment epithelium and Bruch's membrane complex associated with subretinal hemorrhage and subretinal fluid. OCT angiography (Spectralis OCT2 Module; Heidelberg Engineering, Heidelberg, Germany) showed a large well-circumscribed lesion with a hyperintense signal consistent with a choroidal neovascular complex. The area of the choroidal neovascular complex measured using a commercially available external software (Fiji – Image J; ImageJ, US National Institutes of Health, Bethesda, Maryland, USA) was 1.89mm² ( Figure 1 ). Given the presence of subretinal fluid/exudation on structural OCT and presence of a large choroidal neovascular complex on OCT angiography, a diagnosis of active choroidal neovascularization secondary to traumatic choroidal rupture was made. The current standard of treatment for these lesions in the form of anti-VEGF therapy with Bevacizumab^3–5,7,8 was offered to the patient. The patient however refused to receive treatment.

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Figure 1.

(A) color fundus photography of the left eye depicts fovea involving choroidal rupture with overlying subretinal hemorrhage. Yellowish appearing de-hemoglobinized hemorrhage is visible at the edges of fresh hemorrhage. (B) Fundus autofluorescence of the left eye shows a central area of hypoautofluorescence correlating with fovea involving vertical choroidal rupture surrounded by a ring of hyperautofluorescence correlating with the de-hemoglobinized hemorrhage. The juxta-foveal areas of hypoautofluorescence correlate with retinal pigment epithelial degeneration. (C) Structural OCT of the left eye shows a break in retinal pigment epithelium and Bruch's membrane complex (red arrow) associated with a homogenous collection beneath the fovea consistent with subretinal hemorrhage (Green asterisk). Also note the presence of hypointense signal in the parafoveal region consistent with subretinal fluid/exudation (yellow arrow). (D) OCT angiography of the left eye shows a well-circumscribed lesion with a hyperintense signal measuring 1.89mm² (area outlined in yellow). This is consistent with a large choroidal neovascular complex. OCT, optical coherence tomography.

Five weeks later, she presented for follow up in the retina clinic. Her best corrected visual acuity was still counting fingers at two feet in the left eye. Dilated fundus examination and color fundus photography of the left eye showed resolving subretinal hemorrhage overlying the choroidal rupture involving the foveal center. Fundus autofluorescence was consistent with fovea involving choroidal rupture and expanding juxta-foveal areas of retinal pigment epithelial degeneration. Interestingly, structural OCT revealed sub-foveal fibrosis/scarring, improvement in subretinal hemorrhage and complete resolution of subretinal fluid. OCT angiography showed a 2.7 fold reduction in the size of the choroidal neovascular complex, now measuring 0.70mm² ( Figure 2 ). Given spontaneous regression of choroidal neovascular complex on OCT angiography and its quiescence depicted by a complete resolution of subretinal fluid/exudation on structural OCT, a conservative approach without intravitreal anti-VEGF injections was chosen for management.

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Figure 2.

(A) color fundus photography of the left eye depicts fovea involving choroidal rupture with overlying subretinal hemorrhage. The subretinal hemorrhage appears to be resolving and is surrounded by the yellowish de-hemoglobinized hemorrhage. (B) Fundus autofluorescence of the left eye shows a central area of hypoautofluorescence correlating with fovea involving vertical choroidal rupture surrounded by a ring of hyperautofluorescence correlating with the de-hemoglobinized hemorrhage. The juxta-foveal areas of hypoautofluorescence appear to be expanding and correlate with retinal pigment epithelial degeneration. (C) Structural OCT of the left eye shows sub-foveal scarring/fibrosis. The sub-retinal hemorrhage has improved. Note that the parafoveal hypointense signal depicting sub-retinal fluid/exudation previously has completely resolved. (D) OCT angiography of the left eye shows a well-circumscribed lesion with hyperintense signal consistent with a choroidal neovascular complex. Note a 2.7 fold reduction in the size of the lesion to 0.70mm² (area outlined in yellow). This is consistent with regression of the choroidal neovascular complex. OCT, optical coherence tomography.

Conclusion

To the authors’ knowledge this is a first case describing a unique evolution with spontaneous regression and quiescence of choroidal neovascularization secondary to traumatic choroidal rupture without anti-VEGF treatment. OCT angiography was useful in detecting the choroidal neovascular complex early and monitoring its evolution.

A multitude of growth factors including VEGF are implicated in the healing response to traumatic choroidal rupture. Given an upregulation of VEGF, therapy targeted against this growth factor typically with Bevacizumab is the gold standard for managing choroidal neovascularization secondary to traumatic choroidal rupture.^3–5,7,8 Most choroidal neovascular membranes occur in the subfoveal and/or juxtafoveal locations compromising vision. This is likely due to more abundant blood supply and hence a more robust healing response from the choroid in this region.^9,10

The natural history of choroidal rupture associated choroidal neovascularization is spontaneous regression followed by its involution. ⁵ This is probably why typically a small number of injections, usually 1–3, are required to induce quiescence of the choroidal neovascular complex in this condition. ⁵ While anti-VEGF therapy may speed up the process of promoting inactivity of the choroidal neovascular complex, the present case suggests that expectant management may be a viable treatment option for this condition.

In conclusion, the above case shows a spontaneous regression and quiescence of choroidal neovascularization secondary to traumatic choroidal rupture without treatment. OCT angiography serves as a useful tool for early diagnosis of choroidal neovascularization secondary to traumatic choroidal rupture and monitoring the lesion.