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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2589_Библиотеки_им_академика_М_И_Перельмана
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15.3 Evaluation oftheOptic Disc
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15.3.6 Macular OCT inGlaucoma
Nearly 50% of the retinal ganglion cells are in the
macula in a multilayered fashion. Although histopathological studies have shown the loss of RGC,
the advent of OCT technology’s ability to
measure the RGC consistently has focused on the
thickness of the RGC to diagnose early glaucoma. Notably, the RGC layer, the IPL, and the
INL show an age-related decline by 2.8%, 2.1%,
and 0.78% per decade of life [19]. So do the
cRNFL thickness and the minimum neuroretinal
width, but at half the rate making the RGC layer
measurements attractive [19]. There is signicant
thinning of the GCL with increasing the axial
length of the eyeball. The Cirrus HD-OCT (Carl
Zeiss Meditec, Dublin, CA) provides high-speed
acquisition, and a cube scan is done measuring 6
× 6 × 2mm to provide 512 × 128 A-scans centred
on the fovea. It provides a macula GCIPL thickness map of an oval 4.5 × 4mm with the central
1.2 × 1 mm of the foveal centre removed. The
thickness map is provided for six sectors, three
above and three below the horizontal raphe
(Fig.15.4e). A meta-analysis of 150 studies comparing the cRNFL thickness and ganglion cell
inner plexiform layer (GCIPL) found the former
slightly more accurate in diagnosing early or preperimetric glaucoma. However, they performed
equally well with moderate or advanced glaucoma. All ve OCT machines performed equally
well [20]. A vertical asymmetry in the inner retinal thickness is a highly valued tool in diagnosing early glaucoma [21]. Notably, the GCIPL
thickness has ethnic variations, and there is a
need for normative data for different ethnic
groups [22].
15.3.7 Horizontal Raphe Hemield
Test inGlaucoma
ence in the GCIPL above and below the horizontal raphe. It is highly discriminatory in patients
with perimetric or pre-perimetric OAG, even
when the optic disc signs are equivocal. For the
hemield test to be positive, the horizontal line
from the temporal inner and outer annulus should
be detectable for at least over half of the distance; if the thickness difference of the ganglion
cells-inner plexiform layer (GCIPL) is ≥5μm
and if the colour is blue in one half and red/yellow or white in the other half [23]. In older adults
with a large CDR, a positive hemield test predicted the development of normal tension glaucoma years later [24].
15.3.8 OCT Angiography
OCT angiography detects non-invasive movement of red blood cells (RBCs) in the blood vessels. In patients with glaucoma, it shows
decreased supercial capillary vessel density in
the peripapillary and the macular area. It also
shows a lack of choriocapillaris in the parapapillary areas of chorioretinal atrophy [25].
15.3.9 Articial Intelligence
forAutomatic Diagnosis
ofGlaucomatous Optic
Neuropathy(GON)
Given the limited expertise available for interpreting the various OCT parameters for detecting
OAG, attempts have been made to validate 3-D
deep learning techniques for the automatic detection of OAG.The features used for deep learning
were the same as those used by physicians. The
accuracy reached >85%, with high sensitivity
(78–90%) and specicity (79–86%) [26].
The nasal step in visual elds in OAG is a
pathognomonic test of perimetric OAG.In OAG,
the loss of ganglion cells and their axons is
asymmetric above and below the horizontal
raphe. It is responsible for the step-like differ-
15.3.10 Myopia andGON
Myopia frequently accompanies OAG.Myopic
eyes tend to have a shallow temporal rim, a
shelving cup, a myopic crescent, and zone β of
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15 Optic Disc Signs—Cupping, Swelling, Inammation, andPallor
parapapillary chorioretinal atrophy. Zone γ is
seen due to axial elongation of the eyeball in
axial myopia. The fundus is tessellated, and
there is overall thinning and shifting of the
double hump of RNFL. In a multi-task 3-D
model of deep learning, all the information was
gathered about the presence or absence of
myopia features and the SD-OCT ndings in
GON. It will simplify the classication of
GON yes or no and myopic features yes or no
and is likely to be useful in primary care settings [27].
a
bc d
15.4 Choosing aTool forFundus
Examination inNeuroOphthalmological Disorders
A direct ophthalmoscope is a favourite tool of
general physicians for fundus examination
(Fig.15.5A). A large aperture illuminates a 10°
retina view at 15X magnication. Apart from the
raised intracranial pressure, several other pathologies, including vascular and inammatory,
cause swelling of the ONH (Fig. 15.5A–C). To
get a broader view, the examiner has to illuminate
Fig. 15.5 (A) Direct ophthalmoscope view of right (a)
and left (b) eyes, allowing direct 15X but only 5–10° eld
of examination. This patient was referred to as papilledema with a diminution of vision in both eyes for 10
days; the visual acuity was 6/24 and 6/12in the right and
left eyes, respectively. When examined on a +90 D slit
lamp indirect ophthalmoscopy and captured on fundus
camera (c, d) it showed macular edema as the main reason
for vision loss. Further ancillary investigations with combined FFA and ICG angiography (e, f) revealed the presence of bilateral multifocal choroidal granulomas
producing hypouorescent lesions ICG and FFA suggestive of Vogt Koyanagi Harada (VKH) disease, an immunemediated panuveitis. These patients have signs of
meningismus and tinnitus during prodrome and present to
neurologists. A careful fundus examination can prevent
unnecessary neuroimaging and invasive CSF taps. (B) A
34-year-old man presented with vision loss in both eyes
and bilateral optic disc edema (a, b). Fundus uorescein
angiography conrmed optic disc edema (c–f). Note sub-
tle hypouorescent discreet lesions in the background
show late hyper uorescence (White arrows in (d, (e), f).
A slit lamp exam shows keratic precipitates (red arrows in
g, h), ruling out a primary neurological disease. This
prompted a search for inammatory pathology. The tuberculin skin test was negative. His angiotensin-converting
enzyme levels were elevated. The CT scan chest showed
multiple enlarged hilar and mediastinal lymph nodes (Not
shown here). Endobronchial ultrasound-guided lymph
node biopsy revealed epithelioid cell granulomas with
lymphoid aggregation and non-necrotizing inammation
suggestive of Sarcoidosis. (C) A 40-year-old woman presented with bilateral optic disc edema (a–d). Note the
presence of ne new vessels on the optic disc in both eyes,
more marked in the red-free images (b, d) and are silhouetted against a white background in late frames of uorescein angiography (e, f). This patient was also proven to
have sarcoidosis and was treated on oral corticosteroids
with a resolution of the new vessels and optic disc edema
at a one-year follow-up (g, h)
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a
b
Fig. 15.5 (continued)
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15 Optic Disc Signs—Cupping, Swelling, Inammation, andPallor
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bc d
ef
Fig. 15.5 (continued)
various parts of the retina and mentally create a
montage of the retina. There is always a chance
of missing a forest for a tree. The main challenge
in evaluating ONH swelling is determining
whether it is due to an ophthalmological or neurological pathology. Thus, doing a binocular biomicroscopic indirect ophthalmoscopy of the
retina and slit lamp evaluation whenever one
encounters an ONH swelling is advisable especially if the neurological signs are subtle or
absent (Fig.15.5A–C).
Fundus examination is an important step in
the neurological examination. Fundus signs provide signicant diagnostic clues to the physician
before ordering neuroimaging or invasive proce-
dures. In patients with headaches, the absence of
papilledema rules out increased intracranial pressure secondary to intracranial space-occupying
lesions or idiopathic intracranial hypertension
(IIH). On the other hand, visual symptoms with
optic disc pallor may indicate an SOL compressing on the anterior visual pathways.
The retinal signs of hypertension, such as
focal arteriolar narrowing, AV changes, or the
signs of diabetic retinopathy, are related to prevalent stroke, incident stroke, or mortality from
stroke. Retinal arteriolar emboli are related to
stroke mortality (Fig. 15.6) [28]. In a series of
patients referred to the neuro-ophthalmology
clinic, nearly 40% of patients referred with a
15.4 Choosing aTool forFundus Examination inNeuro-Ophthalmological Disorders
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mydriatic camera fundus pictures than direct
ophthalmoscopy [31].
The non-mydriatic camera has been found
superior to direct ophthalmoscopy in neurological patients. Digital images of the fundus also
facilitate a remote consultation with an ophthalmologist [32]. Moreover, digital fundus images
are an excellent tool for teaching neurology residents about detecting and interpreting various
retinal signs crucial to diagnosing and managing
their patients [33].
15.4.1 Optic Nerve Head Edema
andPapilledema-Clinical
Fig. 15.6 Multiple emboli (black arrows) seen as shiny
refractile cholesterol emboli embedded at the bifurcation
of arterioles in a patient with BRAO
diagnosis of IIH did not have IIH.The majority
had already received treatment for IIH.Most of
these patients had abnormal ophthalmoscopy pictures, and all had been subjected to unnecessary
neuro-imaging and spinal taps simply because
they failed to evaluate the optic disc on ophthalmoscopy [29]. Ophthalmoscopy of the
over- diagnosed IIH revealed pseudo papilledema,
ONH drusen, optic atrophy, optic neuritis,
sequential anterior ischaemic optic neuropathy,
and optic nerve hypoplasia [29].
Using a hand-held direct ophthalmoscope is a
signicant challenge for non-initiated resident
doctors. In general, physicians need more condence in doing fundus examinations. Very few
emergency department physicians (14%) perform direct ophthalmoscopy on patients presenting to the emergency department with
neurological symptoms. Under those circumstances, looking at the 45° digital images of the
fundus taken by a non-mydriatic camera is an
appropriate alternative. Thirteen per cent of
patients had signicant positive ndings, detected
on 45° fundus images taken by a non-mydriatic
camera, relevant to the immediate care of the
patients. These included papilledema, optic atrophy, and changes in malignant hypertension [30].
ED physicians are likelier to look at non-
Swelling of the ONH is termed ‘papilledema’
when it results from raised intracranial pressure
(ICP) due to space-occupying lesions, intracranial haemorrhage, central venous thrombosis,
or IIH (Fig. 15.7). Any pathology that leads to
either increased production of CSF or decreased
absorption leads to a rise in ICP. In adults, the
normal ICP in the supine position ranges from 7
to 15mm of Hg. The subarachnoid space of the
brain is continuous with subarachnoid space
around the optic nerve up to the fusion of the dura
mater with the sclera. Thus, any rise in ICP is
transmitted to the subarachnoid space around the
optic nerve compressing the axons pass as they
pass through the lamina cribrosa. At the lamina
cribrosa, posteriorly, the axons are subjected to
pressure in the subarachnoid space and anteriorly
to the IOP.This results in stasis of the retrograde
axoplasmic ow in the axons anterior to the lamina cribrosa. The increased pressure in the ONH
leads to uid leakage from the dilated capillaries,
further compromising the axoplasmic ow.
saving. Usually, papilledema is symmetrical in
both eyes. However, occasionally due to smallsized optic canals, ONH swelling may be asymmetric on one side [34]. Notably, atrophic optic
nerves do not show papilledema even in the presence of raised ICP.The raised ICP may not manifest as papilledema in infants with as-yet open
fontanelles.
Evaluation
The timely diagnosis of papilledema is life-
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15 Optic Disc Signs—Cupping, Swelling, Inammation, andPallor
Fig. 15.7 Papilledema: Bilateral (a, b) swelling of the
optic nerve head (ONH) is termed ‘papilledema’ when it
results from raised intracranial pressure (ICP) due to
Patients with raised ICP often complain of
space-occupying lesions, intracranial hemorrhage, central
venous thrombosis, or idiopathic intracranial
hypertension
15.4.3 Signs ofPapilledema
morning headaches that worsen during coughing
or Valsalva manoeuvre. Headache may be accompanied by vomiting. They may also complain of
diplopia due to sixth nerve paresis as a nonlocalizing sign of raised ICP.Although the visual
acuity may remain normal for a long time, they
may complain of transient obscurations of vision,
especially with a change in posture. Patients may
complain of tinnitus as well.
The first manifestation of papilledema is blurring ofONH margins (Fig.15.7). The margins
of the normal optic disc are finely blurred as
the RNF bundles enter the disc. These fibres
are best seen in red-free light. The normal
blurring of the optic disc needs to be distinguished from the incipient papilledema due to
raised ICP. In nearly 80% of normal people,
spontaneous venous pulsations are visible on
the optic disc. These spontaneous pulsations
15.4.2 Ocular Causes ofONH
Swelling
are abolished if the ICP exceeds 20mm of Hg.
The presence of these pulsations rules out
raised ICP.Notably, venous pulsations may be
Several pathologies in the eye lead to the swelling of the ONH, including central retinal vein
occlusion, malignant hypertension, optic neuritis,
non-arteritic ischaemic optic neuropathy, diabetes, hypotony, posterior scleritis, thyroid ophthalmopathy, inammatory and inltrative diseases
of the ONH by Sarcoidosis, leukemia, lymphoma, metastatic lesions, or orbital pathologies.
Diagnosis of ONH swelling in ocular diseases
does not pose as much of a challenge as in early
cases of papilledema.
absent in 20% of normal people, but can be
elicited by lightly pressing the globe with a
finger. Next is the obscuration of the physio-
logical cup due to axonal swelling. The disc
margins’ blurring is exaggerated in small optic
discs that are otherwise normal, called pseudo
papilledema. In both instances, the optic disc
cup is full/absent. In optic neuritis, the RNFL
may also be seen as coarse, and the ODC may
be absent or partially obliterated (Figs.15.8,
15.9, and 15.10).
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a
b
c
Fig. 15.8 Right eye optic disc is normal (a), while left
eye optic disc shows hyperemia, edema, obliteration of
physiological cup, and tortuous vessels (b). Following
In eyes with pseudopapilledema, the bright
reexes from the large retinal vessels and retina
are seen. Normal RNFL striations are also
visible.
In true papilledema, on the other hand, the
reexes from the large vessels are lost, which
appear dark and dull. The RNFLstriations appear
coarse and obliterated [35]. The swelling of the
neuronal axons rst appears in the inferior and
superior poles of the ONH. On stereoscopic
examination, the ONH is seen elevated. The
height of this elevation can be measured by rst
focusing on the peripapillary retina and followed
by the surface of the ONH with a direct ophthal-
treatment with systemic steroids, the optic disc edema
resolved at 2weeks with mild pallor of optic nerve head
(c)
moscope. A +3D elevation approximates 1mm
of elevation of the ONH.
Persistence of papilledema also leads to congestion of the retinal capillaries, giving the ONH
a hyperemic appearance. The central retinal vein
and its branches appear full and congested.
Linear haemorrhages may be seen on the optic
disc margins (Fig. 15.7). Circumferential folds
around the ONH, termed Paton’s lines, are due to
either retinal wrinkles in the RNFL temporal to
the ONH; outer retina folds when associated with
subretinal uid or, less commonly, choroidal
folds [36]. These are mechanical stress lines
which may be radial, circumferential, or spiral.
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15 Optic Disc Signs—Cupping, Swelling, Inammation, andPallor
Fig. 15.9 (a–d) A 20-Y-O female presented with 3 days
of headache, pain, and loss of vision in BE.Visual acuity
was only the perception of hand motions in the right eye
and counting ngers at 2 meters in the left eye. The right
showed a RAPD.There was signicant opacication of
circumpapillary RNFL R>L.MRI WNL.She was treated
with IV Methylprednisolone. Her vision improved to 6/9
within a week in the left eye. (f–h). Nine months later,
both optic discs showed pallor R>L (e, f). Corresponding
visual elds showed a superior relative paracentral scotoma in the left eye (g) and an inferior Centro-cecal scotoma in the right eye
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Fig. 15.9 (continued)
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Choroidal folds are often seen in patients with
peripapillary scleritis or orbital pathologies. The
subretinal uid can be seen on SD-OCT in the
juxtapapillary area. Cotton wool spots and hard
exudates may be seen in the late stages, forming
a macular fan. Chronically persistent raised ICP
may ultimately lead to secondary optic atrophy
with the pallor of the ONH and astrocytic proliferation on the surface of the ONH, which may
also develop shiny pseudo-drusen-like deposits
from the extruded axoplasm.
Central visual acuity is normal in early papilledema, but if it persists for several months, there
may be a signicant decline in visual acuity, ultimately leading to blindness. In the early stages,
the visual elds show an enlargement of the blind
spot, but in chronic cases, the visual eld starts
showing constricted visual elds.
On fundus uorescein angiography, there is an
initial delay in lling the retinal arterioles but
marked by capillary dilatation in the arteriovenous phase and leakage of the dye in the late
stages. Microaneurysmal dilations may be seen
on the optic disc surface.
15.4.3.1 Clinical Grading
ofPapilledema
Changes in the ONH occur progressively depending upon the severity of the ICP and the duration
of the sustained rise in ICP.Scott etal. [37] used a
modied Friśen scale to grade papilledema. Under
this scale, grade 0 is a normal disc in which the
RNFL follows the ISNT rule, whereby the RNFL
striations are thickest in the inferior sector, followed by the superior, nasal, and temporal sectors.
In larger optic discs, these RNFL striations tend to
be thinner. In grade 1, there is minimal optic disc
edema, and the temporal disc margin is normal; a
subtle halo obscures the underlying retina around
the rest of the disc. In grade 2, this halo surrounds
the optic disc; the nasal disc margins are thickened
but without obscuring emerging vessels from the
disc. In grade 3, the circumferential halo is signicant, and the disc margins are elevated. The blood
vessels are obscure in ≥1 quadrant. In grade 4,
there is obscuration of the retinal vessel segments;
the cup is full, and the disc is elevated with a
marked circumferential halo. In grade 5, all the
vessels on the disc are obscured [37].
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15 Optic Disc Signs—Cupping, Swelling, Inammation, andPallor
a
b
c d
Fig. 15.10 A 28-year-old woman presented with blurred
vision in her left eye for one-day duration. Her visual acuity was 6/6in the right eye and 6/12in the left eye. There
was no RAPD in the left eye. Mild optic disc edema was
noted in the left eye (a). Contrast-enhanced MRI orbit
showed a single lesion in the left optic nerve near the
orbital apex, hypointense on T2 showing ring enhance-
15.4.4 Role ofOCT inPapilledema
Peripapillary RNFL (pRNFL) thickness is
increased in raised ICP. The measurement of
pRNFL in patients with papilledema correlates
with the CSF tap’s opening pressure. Although
the pRNFL thickness is decreased after the control of ICP, its interpretation as a measure of con-
ment (b). A diagnosis of left intraorbital neurocysticercosis with optic neuritis was made. Endoscopic excision of
the cysticercosis was followed by immediate worsening of
vision and disc edema. She was treated on oral albendazole and intravenous followed by oral corticosteroids. She
recovered normal vision and was left with a mild optic
disc pallor (c) and contracted visual elds (d)
trol of ICP needs caution as secondary optic
atrophy due to papilledema also leads to the loss
of RNFL.Thinning of the macular GCIPL layer
is a better indicator for assessing secondary atrophy, as this layer does not show an increase in
thickness with the raised ICP.EDI-OCT can help
differentiate pseudo from true papilledema,
especially in eyes with buried optic disc drusen(ODD) [38].
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