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The choroid: a clearer clinical view

This article provides an overview of choroidal pathology and the application of contemporary imaging techniques used to view the choroid in vivo.


As clinicians, we are very familiar with assessing the health of the retina as part of a routine eye examination, or for follow-up investigation of signs or symptoms. This typically involves direct or binocular indirect ophthalmoscopy, and often fundus photography. In recent years, advanced imaging techniques including optical coherence tomography (OCT) and scanning laser ophthalmoscopy (SLO) have become increasingly common in primary care practice. These devices provide not only a fresh perspective on the posterior eye, but also a clearer view of a structure often previously unseen – the choroid. We discuss how this frequently overlooked structure can provide insights into ocular health.

The choroid is implicated in the pathogenesis of several common ocular conditions, including age-related macular degeneration (AMD), central serous chorioretinopathy, and posterior uveitis. Traditionally, investigation of the choroid relied on histology; an ex vivo technique that cannot be used for diagnosing and monitoring patients. However, advances in imaging technology now allow in vivo investigation of the choroid, with potential for clinical evaluation.

Figure 1

Structure and function

The choroid is one of the most highly vascularised tissues in the body, located between Bruch’s membrane and the sclera. It is comprised of three layers from anterior to posterior: the choriocapillaris (small vessels); Sattler’s layer (medium vessels); and Haller’s layer (large vessels). Anatomically, the choroid is thickest below the fovea, and is thinnest nasally and inferiorly.1,2

The thickness of the healthy choroid varies greatly between individuals with reported mean sub-foveal thicknesses ranging from 196μm to 354μm.1,3–6
The primary function of the choroid is to supply blood to the outer retina with as much as 90% of the oxygen delivered to the retina coming from this source.7 Photoreceptors are highly metabolically active; therefore, supplying sufficient oxygen is a demanding task. This is particularly pertinent at the macula, where the photoreceptors are densely packed to facilitate high acuity vision, and retinal circulation is absent. It has been hypothesised that the fine balance between metabolic demand and limited oxygen supply (in the absence of the dual blood supply) renders the macular region most susceptible to damage.8,9 Other purported functions of the choroid include absorption of stray light by the high melanin content, and contribution to aqueous humour outflow via the uveoscleral pathway.10

Figure 2

Normal variation in the choroid

To make any assessment of choroidal health in the clinic it is important to appreciate the appearance of a healthy choroid and the normal variation in choroidal thickness that one may expect between visits. Both long- and short-term factors have been shown to cause fluctuations in choroidal thickness and blood flow. For instance, studies have identified a relationship between refractive error and choroidal thickness.11,12 The choroid, like the retina, tends to be thinner with increasing degrees of myopia by around 15μm/dioptre.13 Due to the optics of the eye, refractive error and axial eye length (AEL) are also closely related, with high myopes generally having longer eyes. It is, therefore, unsurprising that a link between AEL and choroidal thickness has also been identified with an average thickness decrease of ~50μm per millimetre increase in AEL.14,15

Consumption of coffee (specifically caffeine) has been shown to decrease choroidal thickness by as much as 15%, with the effect lasting at least four hours.16 Consumption of alcohol and large volumes of water have both been shown to cause a small short-term increase in thickness.17,18 Smoking has also been linked to choroidal thickness, although the magnitude and duration of these effects are less clear. A study in 2013 showed a decrease in choroidal thickness of ~30μm (~10%) following the smoking of a single cigarette; a change which persisted for at least three hours.19 The authors suggested a potential link between decreased choroidal blood flow following smoking, and the increased risk of AMD development in smokers, resulting from impaired metabolite supply. 

Figure 3

It is well established that a number of ocular structures undergo diurnal variation, for example, intraocular pressure (IOP), corneal thickness, and AEL. However, it wasn’t until 2009 that a similar variation in choroidal  thickness was observed;20 this fluctuation is generally in anti-phase with the diurnal changes in AEL and may also be associated with oscillations in IOP and the cardiac cycle.21 It is, therefore, clinically important to take into account the time of day when assessing the choroid, much like we would for IOP measurement. 

To summarise, there are multiple factors that can have a significant effect on choroidal thickness. The choroid may appear thicker or thinner on a repeat visit simply due to these physiological differences – for example, the amount of caffeine consumed, or the time of day. These factors should be taken into consideration when assessing the choroid before attributing structural change to pathology. 

The ageing choroid

Ageing affects the choroid in a number of ways. Principally, the choroid becomes thinner with age, reportedly between 1.4-4.1μm/year, although there is great variation between individuals.1,3,22–24 Advancing age also decreases choriocapillaris density and diameter,25–27 and reduces choroidal volume and blood flow.28,29 In addition, increased deposition of oxidised metabolic waste and cross-linking of collagen fibres results in a thickening of Bruch’s membrane with age;30 this reduces the permeability of the membrane, acting as a barrier to diffusion of metabolites between the choroid and outer retina, reducing the metabolic capacity and efficiency. It is thought that this leads to hypoxia in the outer retina and susceptibility to degenerative ageing changes, such as AMD. 

The pathogenesis of AMD is complex and still not fully understood, although it is known to be a multi-factorial condition involving changes to the outer retinal layers, retinal pigment epithelium (RPE), Bruch’s membrane and choroid. Aside from metabolic insufficiency, there are other contributing elements including oxidative stress and chronic inflammation (see Figure 1: A simplified theory of choroidal involvement in AMD pathogenesis, choroidal involvement highlighted).31 The oxidative theory of AMD describes cellular damage to the RPE and choriocapillaris caused by reactive oxygen species in the aged eye; this is the basis for the potential prophylactic effect of high-dose antioxidant supplements, as investigated in the AREDS clinical trials.32 

One of the functions of the RPE is the production of growth factors, including vascular endothelial growth factor (VEGF) and pigment epithelium derived 
factor (PEDF). These have pro- and anti-angiogenic properties, respectively, and play an important role in maintaining choroidal health and structure. An imbalance in these factors caused by RPE dysfunction may lead to development of choroidal neovascular membrane (CNV) if too much VEGF is expressed, or impaired regeneration of the choriocapillaris if too little is expressed, potentially resulting in atrophic change.33 A CNV consists of newly formed vessels originating from the choriocapillaris, which break through Bruch’s membrane into the sub-retinal pigment epithelial space and/or subretinal space (see Figure 2: Conventional spectral-domain OCT b-scans: A) choroidal neovascular membranes in wet AMD appear bright due to their reflective properties; B) geographic atrophy shows a typical thinning and/or loss of the outer retinal layers, RPE and chorocapilaris. More light penetrates beyond the RPE in this area, causing an area of relative hyper-reflectance beneath the atrophy. Note the charateristically thin choroid in this image). These vessels are weak and prone to leakage, resulting in the rapid onset distortion and loss of central vision typical of neovascular (wet) AMD. 

Intravitreal anti-VEGF injections are typically administered every four to six weeks for this disease subtype to reduce expression of VEGF and, therefore, cease further development of the CNV. Although this is widely regarded as an effective therapy, fibrovascular scarring beneath the macula is common resulting from the collection of subretinal fluid and limiting visual acuity recovery. Reports have indicated a reduction in choroidal thickness following a three-month period of anti-VEGF treatment seen with both ranibizumab (Lucentis) and aflibercept (Eylea);34,35 this suggests that intravitreal administration of the anti-VEGF agent targets not only the CNV but also affects the structure of the underlying choroid. 

A significant reduction in choroidal thickness has been identified in patients with AMD, particularly in the late stages of the disease.36–38 In general, eyes with more drusen have a thinner choroid, suggesting a link between impaired metabolic waste removal and decreased choroidal blood flow.39 Choroidal thinning has also been linked to a number of systemic factors, particularly cardiovascular-associated conditions including hypertension, obesity, and diabetes mellitus.40–42 It is interesting to note that all of these are identified risk factors for late-stage AMD, which raises a classic causation-correlation debate: is a thinner choroid caused by AMD, is it a predisposing risk factor for AMD, or is it simply a manifestation of the associated confounding factors? Regardless of the nature of this relationship, a thinner choroid is easily observed by clinicians in most OCT scans from conventional devices (see Figure 2), and can be associated with development of late-stage AMD. 

Figure 4

Other pathologies affecting the choroid 

In contrast, some ocular conditions are associated with a thicker choroid. Firstly, and perhaps unsurprisingly, choroidal thickness increases in active posterior uveitis (see Figure 3: SS-OCT imnage of posterior uveitis of unknown origin. Note the thick choroid and vitreous inflammation).43,44 Also known as choroiditis, this is an inflammation of the choroid that may also involve surrounding structures such as the retina (retinitis) and vitreous (vitritis). Posterior uveitis is often a manifestation of an underlying systemic inflammatory condition, such as sarcoidosis, Vogt-Koyanagi-Harada (VKH) syndrome, or Behçet’s disease. In the inactive stage of chronic uveitis, a reduction in choroidal thickness and choroidal vessel diameter is observed.45 

Central serous chorioretinopathy (CSC) is an idiopathic condition causing a detachment of the retinal layers from the RPE at the macula, allowing fluid from the choroid to collect in the subretinal space (see Figure 4: SS-OCT image of central serous chorioretinopathy. Subretinal fluid appears dark due to low reflectivity). Also known as central serous retinopathy (CSR), it most commonly affects males aged 20–50, and is thought to be associated with stress. The choroid is typically very thick in these patients, in the region of 421–505μm in the affected eye (as much as double that of the average choroid).46–48 Interestingly, the choroid tends to be thicker than normal in the fellow eye, even if the chorioretinopathy is observed unilaterally (around 324μm-387μm in the unaffected eye);47,48 this may be caused by choroidal hyperpermeability and increased hydrostatic pressure in the choroid, which could potentially be linked to stress. In healthy eyes, the choroid is ~18% thicker in men than women, which may in part explain the sex-linked prevalence of CSC.14 

Figure 5a

Imaging the choroid 

We know that the choroid changes in many ocular diseases, but how do we examine this structure in the clinic? The location of the choroid, beneath the retinal layers and highly pigmented RPE, makes it difficult to view in vivo. Melanin pigment is highly scattering and absorbing, restricting visibility of choroidal vessels, particularly at the macula where pigment density is highest. There is less pigment in the peripheral retina of healthy eyes, resulting in the commonly seen tigroid fundus appearance (see Figure 5A: Optomap images of an eye with a choroidal naevus: A) widefield composite view); this appearance is typically accentuated in eyes with depigmentation, such as in high myopia or retinal atrophy. Despite our restricted view of the choroid in the majority of patients using ophthalmoscopy, contemporary imaging techniques allow high-resolution investigation of the choroid in optometric practice. 

Invasive imaging techniques 

Intravenous injection of contrast material can be used to enhance the appearance of vascular structures, similar to methods used for CT scans of various organs. Commonly used ophthalmic imaging techniques requiring systemic administration of contrast material are fluorescein angiography (FA) and indocyanine green angiography (ICGA). Modified fundus cameras utilising exciter and barrier filters are used to collect a series of images as the contrast material fills and empties from the retinal and choroidal vessels. Hyperfluorescent areas are indicative of leaking defects, for example, neovascularisation secondary to AMD or diabetic retinopathy, and hypofluorescent areas suggest a blocking or filling defect as in cases of retinal artery occlusion. The period between injection of dye and fluorescent stages can be used to estimate rate of blood flow through the vasculature. 

ICG fluoresces in the near infrared range (longer wavelength light), which penetrates pigmented structures more efficiently, producing an advantage for imaging structures beneath the RPE. Both FA and ICGA carry small risks associated with introduction of foreign material, including anaphylaxis. Furthermore, ICG preparation contains sodium iodine, and an intolerance test should be carried out prior to use. Due to the invasive nature of these methods, their use is limited to secondary care. 

Figure 5b

Non-invasive imaging techniques

Optical coherence tomography (OCT) is the optical analogue of ultrasound, measuring backscattered light from the ocular structures. This produces far higher imaging resolution, resulting in detailed views of the retinal layers and choroidal vessels. Advances in OCT technology now allow an optimised view of the deeper retinal layers and choroid, which previously had only been possible ex vivo. Enhanced depth imaging (EDI) reduces the distance of the OCT device from the eye, effectively inverting the image and positioning the plane of focus closer to the choroid;49 concentration of the focused light at this plane increases visibility of the deeper structures. This facility is included in the on-board software of several commercial OCT devices, including the Cirrus HD-OCT (Carl Zeiss Meditec, Inc., Dublin, CA) and Spectralis (Heidelberg Engineering, Heidelberg, Germany). 

Although the majority of OCT devices operate at around 800–860nm, longer wavelengths of light are less affected by scatter; this improves visualisation beneath the RPE,50 and reduces image degradation caused by media opacities, such as cataract.50 The only commercially available long-wavelength (1050nm) OCT was launched in Europe in March 2015; the DRI OCT Triton (Topcon Corp, Tokyo, Japan; see Figures 3 and 4). This device also utilises swept source technology (SS-OCT) to reduce signal loss with increasing imaging depth, which further improves visualisation beneath the RPE, and renders EDI unnecessary for SS-OCT devices. The on-board analysis software of the DRI OCT Triton produces automated identification of the anterior and posterior choroidal boundaries on the scans, producing choroidal thickness maps for quick interpretation, like those typically seen for retinal thickness on many OCT devices. 

The ultra-wide field Optomap (Optos plc, Dunfermline, Fife, UK) makes use of wavelength-dependent scatter. Scanning laser ophthalmoscopy is used to capture 200° retinal images, compared to the typical 45° fundus photograph, or the 20° OCT volume scan. It does not produce cross-sectional images like OCT, but uses two light sources at different wavelengths (red and green) to improve colour contrast and provide depth cues for retinal features, based upon the relative absorption of each wavelength by the structures. The majority of information obtained by the green laser pertains to the sensory (inner) retina, while the red laser (longer wavelength) predominantly represents the RPE and choroid. The images from each laser can be separated or viewed simultaneously. In the green laser separation, features like retinal haemorrhages are enhanced (akin to a red-free filter), while in the red laser separation, deeper features such as choroidal vessels and naevi may be accentuated (see Figure 5: Optomap images of an eye with a choroidal naevus: A) widefield composite view; B) red separation enhances the lesion and choroidal vessels; C) the retinal vessels are defined on green separation). 

Optical coherence tomography angiography (OCTA) is a more recent addition to the ocular imaging market. It employs motion contrast to identify blood flow, by comparing backscattered signal in sequential OCT images. Areas with no difference between repeated scans are deemed stationary, while differences in appearance are attributed to motion caused by blood flow. Both the retinal and choroidal microvasculature may be viewed with OCTA, and volume scans are produced in a matter of seconds. No injection of contrast material is required for this technique, providing advantages over traditional FA and ICGA. However, since this technique requires motion to identify vessels, stationary fluid leakage cannot be detected as with other angiography techniques. 

Despite this, OCTA has been shown to be capable of detecting changes in choroidal blood flow, indicating the presence of CNV in AMD, and capturing microvascular abnormalities in diabetic eyes and vascular occlusions.51 Much research is ongoing in the field, and OCTA shows promise for future use in identifying changes to the vasculature seen in ocular pathologies. 

Figure 5c


Due to the previous limitations in clinical examination of the choroid, its role in ocular pathology has traditionally been given little attention. However, advances in imaging technology mean we are now capable of viewing the structure in high resolution. With vascular changes now detectable using quick, non-invasive clinical imaging techniques, the choroid has been implicated in the pathophysiology of a number of common degenerative and inflammatory ocular pathologies. An appreciation of choroidal thickness may aid clinicians in detecting and assessing risk of developing these common conditions. With modern imaging devices such as OCT becoming commonplace in the primary care setting, perhaps we should no longer be so quick to overlook the choroid, and what it can tell us. 

About the authors

Louise Terry BSc, MCOptom, AFHEA graduated from Cardiff University in 2012 with a BSc in optometry. She is currently a clinical supervisor and PhD student at Cardiff University, investigating changes to the choroid in AMD. 

Dr Ashley Wood PhD, BSc, FHEA graduated from Cardiff University in 2006 with a BSc in optometry and received his PhD in 2011. He is currently a lecturer in the School of Optometry and Vision Sciences, Cardiff University, with research interests in AMD and ocular imaging. 


DRI OCT Triton (SS-OCT) images courtesy of Dr Carl Glittenberg, Topcon Corporation and Karl Landsteiner Institute for Retinal Research 
and Imaging; and Professor Paulo Stanga, Manchester Royal Eye Hospital. Optomap retinal images courtesy of Optos plc. 


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