Choroidal folds were first described by Nettleship in 1884 in a patient with papilloedema due to a space-occupying lesion. Choroidal folds appear as a series of subretinal alternating dark and bright lines, grooves, or striae. They are usually arranged parallelly in a horizontal fashion but can be vertical, oblique, circumferential, or irregular. They rarely extend beyond the equator. They may be unilateral or bilateral. The folds usually broaden with time, becoming smoother and whiter in appearance. In the early stages, they may be as narrow as small blood vessels but gradually become wider with smoother edges. When the neurosensory retina is also involved in the fold, it is called a chorioretinal fold.
Broadly, the conditions associated with choroidal folds are:
The suggested etiologies depend on associated conditions and are as follows:
The characteristic striations seen in the case of choroidal folds are thought to be due to choriocapillaris congestion along with its attachment to overlying Bruch’s membrane. In the absence of these attachments and congestion of the choriocapillaris, the retinal pigment epithelium can slip over the choriocapillaris. This will prevent choroidal fold formation.
There are no prevalence figures available on the occurrence of choroidal folds in the general population.
Patients may be asymptomatic or may complain of worsened visual acuity or metamorphopsia. Patients may be asymptomatic when mild choroidal folds develop. Visual dysfunction is more common in acutely developed choroidal folds. Patients with long-standing folds usually have normal visual acuity.
On ocular examination, choroidal folds are visualized, which are best appreciated with a slit lamp and +90D or +78D lens. A red-free filter accentuates the appearance of folds.
Other relevant ocular and systemic history, according to the associated condition may be present.
In cases of idiopathic choroidal folds, the most common type, patients are invariably asymptomatic males that present with presbyopia. These cases usually have hyperopia. The choroidal folds can be either bilaterally symmetrical or occur in one eye, followed by the involvement of another eye during the observation period. The folds are usually bilaterally symmetrical, parallel, and confined to an area above and below the optic disc and macula. Such cases may represent uveal effusion syndrome, previous episode of posterior scleritis, and increased intracranial tension, therefore all possible causes must be excluded before labeling a case as 'idiopathic'.
Cases of acquired hyperopia with choroidal folds are usually in males and are detected on routine examination or with a complaint of blurred vision. Along with choroidal folds, they may be associated with ophthalmic findings such as mild disc swelling, focal retinal pigment epithelial defects, phoria or tropia, and central serous pigment epitheliopathy.
In the case of choroidal tumors, the choroidal folds surround the tumor base. Since the tumor stretches the overlying choroid, there are no folds above the choroidal tumor.
The intraocular pressure is usually less than 6 mm of Hg in choroidal folds related to hypotony. The choroidal folds are broad and randomly oriented. Other signs of hypotony include tortuous and engorged retinal vessels, stellate folds around the center of the fovea, and rarely cystoid macular edema.
In the case of nanophthalmos, patients have small hyperopic eyes which are in a deep orbit with narrow palpebral fissure. Other features include an elevated papillomacular bundle, retinal fold, pigmentary retinopathy, and macular holes.
Cases of papilledema usually present with symptoms of headache, nausea, vomiting, and sometimes with associated transient visual obscurations. The fundus examination usually shows papilledema and choroidal folds concentric to the disc along with horizontal choroidal folds over the macula, which converge towards the nasal margin of the optic disc.
A scleral buckle is usually placed in cases of rhegmatogenous retinal detachment. Choroidal folds in such cases are usually formed near the posterior slope of the buckle.
Cases of uveal effusion have a waxing and waning clinical course. The choroidal folds are associated with serous choroidal detachment. Sometimes these cases would just have choroidal folds as the initial sign. Other associated features include dilated episcleral vessels, presence of few vitreous cells, intraocular pressure within the normal range, retinal pigment epithelial changes, and exudative retinal detachment with shifting fluid.
Cases of posterior scleritis present with a unilateral decrease in vision with severe pain (may not allow the patient to sleep or may awaken the patient from sleep), mild proptosis, and restricted ocular movements with pain during ocular movements. These patients may have a history of rheumatoid arthritis, collagen vascular diseases, or other autoimmune diseases. The ocular examination usually reveals a localized choroidal elevation, which is surrounded by concentric choroidal folds.
VKH disease usually has a clinical course passing through the following stages: prodromal phase, acute uveitic phase, convalescent phase, and chronic recurrent phase. The prodromal phase manifests as tinnitus, ocular pain, low-grade fever, photophobia, and nuchal rigidity. The acute uveitic phase manifests as a visual loss with fundus findings of choroidal folds, exudative retinal detachment, disc edema, and Dalen-Fuchs nodules. The acute uveitic phase is followed by the convalescent-phase, which itself manifests as alopecia, poliosis, and vitiligo with depigmentation of choroid giving a ‘sunset glow fundus’. The chronic recurrent phase is characterized by cataract, glaucoma, or choroidal neovascularisation.
SANS is seen in astronauts who usually present with hyperopic refractive error, disc edema, choroidal folds, and retinal cotton-wool spots after long-duration space travel.
In the case of intra-conal lesions, patients usually have hyperopia, whereas extra-conal lesions lead to astigmatism. In cases of orbital lesions, a choroidal fold pattern gives us a clue to localize the lesion.
Choroidal folds have a variable pattern depending on whether the orbital lesions are intra-conal or extra-conal.
Fundus fluorescein angiography (FFA) demonstrates more severe fundus changes than routine slit-lamp examination. After fluorescein injection, the peaks fluoresce, and the troughs remain dark. The peaks and troughs can be better contrasted during the subsequent arterial and venous phases when they appear as alternating bright and dark lines, but there is no leakage. More folds are detected on fluorescein angiography as compared to light ophthalmoscopy.
FFA in cases of VKH disease shows pinpoints of hyperfluorescence, which in later stages of disease show pooling surrounded by a dark rim.
CSCR shows leakage in a characteristic inkblot or smokestack or diffuse leak pattern on FFA.
FFA in choroidal metastasis helps in assessing the size of the lesion and identifying flat lesions of choroidal invasion, which would have been missed on clinical examination. They are hyperfluorescent in the early phase, which becomes hyperfluorescent in the late phase. Tumor border shows dilated retinal capillaries with pinpoint leakage in many cases.
Indocyanine green angiography (ICGA) may help to examine the choroidal conditions associated with choroidal folds. VKH disease in its acute phase shows hyperfluorescent dark dots, early hyperfluorescent choroidal stromal vessels, and fuzzy stromal vessels. Central serous chorioretinopathy (CSCR) shows delayed choroidal filling along with hyperfluorescent areas in the early phase, choroidal hyperpermeability leading to geographic areas of hyperfluorescence in mid-phase with persistent hyperfluorescence or washout in the late phase. Mid and late phases in the active cases of CSCR are associated with punctate hyperfluorescence.
Ultrasound B scan (USG) is a non-invasive technique which does not detect choroidal folds but demonstrates flattening and thickening of the posterior sclera and choroid. It provides characteristic images in cases of choroidal mass, retrobulbar mass, posterior scleritis, and other conditions. It also helps in determining axial length to diagnose nanophthalmos. It can measure the choroidal thickness and the flattening of the posterior pole in cases of orbital mass.
USG is a very important tool in the diagnosis of posterior scleritis in which posterior coats of the eye appear thickened and flattened. Other common findings are retrobulbar edema, ‘T’ sign if the retrobulbar edema surrounds the optic nerve, retinal detachment, distension of optic nerve sheath, optic disc swelling, and scleral nodules.
Optical coherence tomography (OCT) shows the presence of undulating retinal pigment epithelium in cases of choroidal folds. Associated OCT findings in CSCR include neurosensory detachment, usually with pigment epithelial detachment. VKH shows characteristic multilobular outer retinal/subretinal serous exudates pooling with septa, which are considered to be highly diagnostic.
OCT angiography may help to find out the role of abnormal blood flow in the pathophysiology of choroidal folds.
Blood pressure should be measured in all cases of papilledema to rule out accelerated hypertension.
Radiological investigations like CT scan and MRI may often be necessary to investigate an underlying condition. For example, idiopathic intracranial hypertension in cases of acquired hyperopia where variable enlargement of the optic nerve image, flattening of the posterior pole of affected eyes, and sometimes a discernible space between the nerve and its sheath is seen.
Invasive procedures like lumbar puncture may be required in selected cases. Uveal effusion may show an increase in the cerebrospinal fluid (CSF) protein level and increased CSF pressure without pleocytosis. VKH may show CSF pleocytosis in the prodromal stage. Some authorities recommend that lumbar puncture should be performed before labeling a case as idiopathic, especially if imaging is unremarkable to rule to high intracranial pressure.
Since choroidal folds can be associated with thyroid orbitopathy, thyroid function tests can be done in suspected cases.
Unilateral cases of choroidal folds have a higher chance of orbital disease and more severe ocular disease than bilateral presentations. Management should be directed towards treating the underlying cause. The diagnosis of the underlying pathologic situations leading to choroidal folds can become challenging. A proper tailored approach taking into consideration the specific features of each case is necessary so that potentially serious and treatable conditions are diagnosed with optimal investigations.
Idiopathic cases can be observed as they are usually asymptomatic. Cases of acquired hyperopia with choroidal folds can usually be observed as no active treatment is required. Management of choroidal tumors varies depending on the suspected tumor.
Observation with lifestyle modification is usually the first line of treatment in most cases of CSCR. Chronic or recurrent cases can be treated with argon laser or green 532 nm frequency-doubled Nd-YAG laser photocoagulation, or micropulse diode laser to point of leakage. Photodynamic therapy is another modality. Carbonic anhydrase inhibitors and anti-corticosteroid therapy have also been tried with variable results.
Cases of severe uveal effusion can be treated with scleral flaps excision and decompression of vortex veins. Nanophthalmic or smaller eyes have a high risk of developing complications like uveal effusion and angle-closure glaucoma. Management in such cases should be directed towards treating the complications. Angle-closure glaucoma can be treated with laser iridotomy, trabeculectomy, or pars plana lensectomy with vitrectomy.
Cases of papilledema should be evaluated for causes of raised intracranial tension and managed accordingly.
Management in cases of hypotony should be directed to find out the underlying cause. Posterior scleritis cases can be started with oral analgesics and corticosteroids. Refractory cases can be given intravenous corticosteroids. High dose systemic corticosteroids and immunomodulatory therapy are important in the management of VKH disease. Cases of active choroidal neovascularization are treated with anti-VEGF (vascular endothelial growth factor) agents. Choroidal scars may be observed. Cases of space flight-associated neuro-ocular syndrome should be managed similarly to papilledema. Space anticipation glasses can be used to counteract the hyperopic shift on the International Space Station. Acetazolamide and venoconstrictor thigh cuffs to counteract cephalad shift of fluid and lower body negative pressure techniques have also been tried. Management of cases with orbital lesions should be done as per the identified lesion. Management of orbital cellulitis and chronic sinusitis centers around treating these conditions with broad-spectrum antibiotics for at least 2 to 3 weeks.
Management of Graves ophthalmopathy requires a multidisciplinary approach of both endocrinologists and ophthalmologists. Though converting the patient to a euthyroid state is important, it is not necessary if ophthalmic complaints require urgent treatment. Hyperthyroidism can be treated with anti-thyroid drugs, radioactive iodine, or thyroidectomy. Graves’ ophthalmopathy can be treated with supportive measures like lubricants and smoking cessation. Corticosteroids and radiation therapy can also be tried. Surgery may be done for orbital decompression, strabismus, and eyelid retraction.
Retinal folds which can accompany choroidal folds are important in the differential diagnosis. Retinal folds usually have a normal fluorescein pattern. Retinal folds are usually narrower than choroidal folds, and they seem to radiate from pathological lesions in the retina. There is usually an abnormal vitreous or vitreoretinal interface associated with it. They may show increased tortuosity of retinal blood vessels. Retinal folds may occur with an epiretinal membrane, subretinal scar, subretinal neovascular membrane, subretinal fluid, uveal or scleral thickening, or with optic nerve disease. Retinal pigment epithelial folds commonly occur with choroidal folds and are found in cases of macular degeneration and appear as fine pigmentation lines alternating with light orange. They look like thick, wrinkled cloth on slit-lamp biomicroscopy. It is specifically associated with pigment epithelial detachment and subretinal neovascularization.
Chorioretinal folds can lead to maculopathy which has been staged with the help of FFA into:
The fluorescein pattern in stage 3 is similar to the late leakage of the undetermined source described in the macular photocoagulation study.
Prognosis in the case of choroidal folds depends upon the associated underlying conditions:
Focal RPE defects can develop along the choroidal folds which can later be associated with choroidal neovascularisation. Hence, careful monitoring is required at regular intervals.
The patient should be appropriately counseled regarding the prognosis of choroidal folds. Idiopathic cases require observation. Most other cases require work-up and management as per the etiology detected.
Any patient presenting with choroidal folds should not receive treatment by an ophthalmologist in isolation. It requires an interprofessional team evaluation by various specialists, including endocrinologists, neurologists, and otolaryngologists. Interprofessional communication can lead to better patient management. The patient will most often present to the primary provider, and these professionals should be aware of the condition as it is treatable. Prompt referral to an ophthalmologist is necessary. These patients can then be followed by their primary clinicians and should ensure compliance with treatment. Pharmacists can ensure correct dosing on the medication management aspect of the condition. Nursing will be the first to come in contact with patients on followup and can assess treatment progress as well as evaluate compliance with both medication and lifestyle measures, and report any issues to the primary care provider. This collaborative, interprofessional approach to care can ensure optimal patient outcomes. [Level 5]
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