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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5528_Библиотеки_им_академика_М_И_Перельмана.pdf
10 N. Shah & A. Orlin
The first OCT technology developed was the time domain (TD) OCT
(Stratus OCT, Carl Zeiss Meditec) which used a mobile reference arm
mirror to measure light echoes from time delays and has acquisition speeds
of 400 A scans/second and axial resolution of up to 810 microns.
2,3
More
recently, spectral domain (SD) OCT (Cirrus HD-OCT, Carl Zeiss Meditec;
Spectralis OCT, Heidelberg Engineering) was developed to provide higher
acquisition speeds of 25,000–52,000 A/scans per second and improved
axial resolution of 37 microns with less motion artifact and much better
visualization of the retinal layers.
2,3
The latest OCT technology allows for complete visualization of the
retina and deeper tissue structures. Some of these new devices include
enhanced depth imaging (EDI) to visualize choroidal pathology, en face
OCT to provide a frontal view of the retinal plane, and OCT angiog-
3
raphy to visualize retinal and choroidal blood vessels.
While not yet
widely commercially available, the swept source (SS) OCT (DRI OCT,Topcon) obtains 100,000–400,000 A scans/second, allowing for 5.3µm tissue
resolution.
2,3
Optical Coherence Tomography: Clinical Applications
The applications of OCT are endless. In addition to diagnosing and managing retinal disease, which is the focus of this chapter, OCT imaging is
also used to visualize the anatomy of the anterior segment (cornea, angle,
lens, and anterior chamber) and the optic nerve.
Normal retinal anatomy
The retina consists of a series of neurons with their cell bodies and axons
ultimately forming the fibers of the optic nerve, which travel to the brain
and a llow visual perception. There are nine layers to the normal retina
which is bordered by the vitreous cavity anteriorly and the retinal pigment epithelium (RPE) and choroid posteriorly (Figure 1, labeled normal
retina, all layers labeled). The innermost, anterior structure of the retina is
the internal limiting membrane (ILM) and consists of the Muller cell foot
Eye, Posterior 11
NFL
OPL
XLM
ONL
EZ
Choroid
Figure 1. Normal retinal OCT with layers labeled.
GCL
IPL
INL
RPE
processes and its basement membrane.4The Muller cells are located in the
middle layers of the retina and serve as a supportive, structural cell to the
4
retina.
Underneath the ILM is the retinal nerve fiber layer (RNFL)4which
is composed of axons from the cell layer directly below it: the ganglion cell
4
layer (GCL).
The ganglion cell neurons receive visual information from
the photoreceptor cells, which are then transmitted to the brain via the optic
nerve. Below the GCL is the inner plexiform layer (IPL), which forms the
axons for the inner nuclear layer (INL).
4
The Muller cell bodies are found
in the INL, as well as cell bodies for other supportive structural and signaling pathway cells. Underneath the INL is the outer plexiform layer (OPL),
which consists of axons of the outer nuclear layer (ONL) where the pho-
4
toreceptor nuclei lie.
The external limiting membrane (XLM) lies below
the ONL. The outer retinal layers include the ellipsoid zone (EZ) and interdigitation zone which represent components of photoreceptor anatomy.
Below the neurosensory retina is the retinal pigment epithelium (RPE),
which acts as the dividing line between the retina and choroid.
4
The choriocapillaris — the most superficial blood vessels of the choroid plexus —
lies just under the RPE.
4
The macula is the area of the retina just temporal
the optic nerve, which the OCT will typically capture, and is responsible for
a patient’s central vision. The fovea is a small central pit within the macula
where vision is sharpest (Figure 2, fundus photo of macula, fovea labeled).
The two main areas of vascularization of the retina include the central retinal artery (CRA) which supplies the superficial inner part of the retina
and the choriocapillaris from the choroid which supplies the outer retina.
4
12 N. Shah & A. Orlin
Macula
Fovea
Figure 2. Fundus photo of retina, macula labeled.
Optic Nerve
This distinction is important as diseases affecting the retinal circulation
typically cause inner retinal findings, whereas those affecting the choroid
may manifest initially in the outer retina.
Retinal vascular disease: Diabetes, retinal vein, and artery occlusions
Just as many systemic vascular disorders including diabetes and hypertension can affect blood vessels in the rest of the body, they damage the retinal
vascular circulation as well. With continued vascular injury, exudate and
fluid can leak out of the injured vessels into the retina causing cystic spaces,
known as macular edema. In the diabetic population, this is referred to as
diabetic macular edema (Figure 3(a),DME), although itcan occur in various
other retinal vascularconditions, such as retinal vein occlusion (Figure 4(a),
RVO edema). These processes are in part mediated by vascular endothelial
Eye, Posterior 13
(a)
(b)
Figure 3. (a) Diabetic macular edema with cystoid spaces (arrow). (b) Resolved following therapy.
(a)
(b)
Figure 4. (a) Retinal vein occlusion with cystoid spaces in the inner retina (arrow). (b) Resolved
edema following therapy (straight arrow).
14 N. Shah & A. Orlin
growth factor (VEGF). The edema is a leading cause of vision loss, particularly among diabetic patients, and is treated most commonly by continued
anti-VEGF intravitreal injection therapy, such as ranibizumab, aflibercept,
or bevacizumab. OCT is not only important in diagnosing edema related to
these various retinal vascular conditions but is also crucial in monitoring
the progression and disease response to treatment which assists the physician in determining the treatment regime (Figures 3(b) and 4(b), response
to treatment in DME and RVO).
Central retinal artery occlusion can occur following an embolic event
and can lead to profound vision loss. Acutely the inner layers of the retina
(supplied by the CRA) appear hyperreflectivebut laterbecome ischemic and
atrophied (Figure 5(a) and (b), CRAO acute vs chronic). Any retinal vascular disease associated with ischemia can lead to the risk of the development
of abnormal blood vessels in the retina — retinal neovascularization — and
subsequent complicationsinclude vitreous hemorrhage,retinal detachment,
and glaucoma.
Choroidal disease: Age-related macular degeneration, myopic degeneration, and central serous chorioretinopathy (CSR)
The leading cause of blindness in the United States in those 50 years of
age or older is age-related macular degeneration (AMD), a disease in part
due to abnormality in the choroid.
early on by the deposition of granular, lipid-rich material called “drusen”
on the surface of the RPE (Figure 6, dry AMD with drusen). As AMD
progresses, it can lead to vision loss from either (1) neovascular AMD (i.e.
“wet” macular degeneration)or (2) geographic atrophy related to dry AMD.
Neovascularor wet AMD is responsible for the majority of the acute central
vision loss that occurs in AMD. With wet conversion, abnormal choroidal
blood vessels from underneath the retina can lead to hemorrhage or exudation under the RPE or in the subretinal and intraretinal space (Figure 7(a),
CNVM pre Rx). These abnormal blood vessels are referred to as choroidal
neovascular membranes (CNVMs). Untreated, CNVM can lead to scarring
and significant central vision loss. Fortunately, with the advent of multiple antivascular endothelial growth factor (VEGF) therapies over the last
4
Macular degeneration is characterized
(b)
Eye, Posterior 15
(a)
Figure 5. (a) Acute hyperreflective changes from retinal artery occlusion (arrow). (b) Long-term inner
retinal ischemia/atrophy (arrow).
Figure 6. Nonexudative age-related macular degeneration, with drusenoid deposit along the RPE
(arrow).
16 N. Shah & A. Orlin
(a)
(b)
Figure 7. (a) Exudative age-related macular degeneration with subretinal fluid (straight arrow) overactive choroidal neovascular membrane (dashed arrow). (b) Fluid resolution following therapy with
residual subretinal scar (arrow).
decade, many patients are able to preserve and maintain visual acuities of
20/40 or better with injection therapy and respond well to treatment (see
Figure 7(b), CNVM post Rx).
5–8
CNVM is most commonly caused by AMD but can result from other
diseases as well. High myopia can result in CNVM through anatomic thinning of the retina and underlying choroid, resulting in breaks in Bruch’s
membrane that create a conduit for new blood vessels to grow, leak, and
cause visual distortion which also respond well to anti-VEGF therapy
(Figure 8(a) and (b), myopic CNVM, pre and post Rx, highly thin myopic
choroid). The myopic fundus is different than the patient with AMD in
that there are no drusen and the choroid is particularly thin. Other features of myopic fundi on OCT may include downward staphylomatous
bowing (Figure 9, myopic staphyloma) and myopic retinoschisis which is
Eye, Posterior 17
(a)
(b)
Figure 8. (a) Myopic choroidal neovascular membrane (arrow). (b) Resolution following therapy.
Figure 9. Myopic staphyloma with posterior displacement of retina, choroid, and sclera (arrow).
characterized by splitting of the layers of the retina (Figure 10, myopic
schisis). These features are not typically visually significant.
Another commonly seen chorioretinal disease is a condition called
central serous chorioretinopathy. This disease typically affects middle-aged
18 N. Shah & A. Orlin
Figure 10. Myopic macular schisis with splitting of the retina in the inner and outer nuclear layers
(arrow).
men and is characterized by well-serous detachments of the retina and
RPE (Figure 11(a)). The pathology is thought to be related to poor pump
4
function of the RPE and defects in the choriocapillaris.
EDI OCT shows
choroidal thickening in these patients and is associated with steroid use,
stress, or type A personality. Fortunately, the majority of these patients
improvespontaneously without treatment(see Figure 11(b)), which is easily
monitored with OCT .
Macular pucker and hole
A macular pucker, also known as an epiretinal membrane (ERM), consists
of a sheet of glial tissue that overlies the ILM. An ERM develops slowly
over time and is relatively common; 20% of those over 75 years old have
4
this pathology on exam.
the retina, leading to foveal distortion (Figure 12(a), ERM symptomatic).
This may result in metamorphopsia or central vision distortion which is
treated with vitrectomy surgery and ERM removal (see Figure 12(b)).
Treatment decision-making is based on exam, OCT, and clinical history as not all patients with ERMs are symptomatic and may be simply
observed.
Superficial traction forces from an ERM or vitreous can also lead to
macular hole formation. Smaller macular holes can spontaneously close
Advanced ERM can cause underlying traction on
Eye, Posterior 19
(a)
(b)
Figure 11. (a) Serous subretinal fluid (straight arrow) in central serous chorioretinopathy. (b) Resolved
fluid with observation.
(Figure 13(a) and (b)) although larger ones typically require surgical repair
(Figure 14(a) and (b), large FTMH s/p repair). Lamellar holes are partial,
non-full thickness, macular holes or “pseudoholes” and typically do not
require surgical intervention as they are visually insignificant. They appear
similar to full-thickness macular holes on exam and are more easily differentiated with OCT (Figure 15, lamellar hole).
Hereditary retinal dystrophies: Retinitis pigmentosa, Stargardt’s disease
There are numerous hereditary retinal dystrophies and degenerations that
cause varying degrees of vision loss, from asymptomatic disease to severe